Opening the book…
Figure 2.1: Global HIV/AIDS Prevalence and HIV Interaction with an Immune Cell
This image is a two-panel image. Panel (a) shows a world map of HIV/AIDS prevalence by country, and Panel (b) shows a color-enhanced microscopic image of HIV particles interacting with a human immune cell.
Panel (a): World Map of HIV/AIDS Prevalence
This panel displays a global map in which countries are color-coded according to the percentage of the population living with HIV/AIDS.
- Dark red indicates the highest prevalence, greater than 20%, concentrated primarily in southern Africa.
- Red and orange shades indicate prevalence levels between approximately 5% and 20%, also concentrated largely in sub-Saharan Africa.
- Yellow indicates prevalence levels between approximately 0.5% and 2%.
- Light green indicates prevalence levels between approximately 0.1% and 0.5%.
- Yellow-green indicates prevalence levels below 0.1%.
- Gray-green indicates countries categorized as AIDS-free. Examples include Australia, New Zealand, and Japan.
- Pale blue-gray indicates No data available. An example shown on the map is Greenland.
Overall, the map highlights that HIV/AIDS prevalence is substantially higher in parts of Africa than in most other regions of the world. Southern Africa contains the highest concentrations of countries with prevalence rates above 15% and 20%, while much of North America, Europe, Asia, South America, and Oceania have substantially lower prevalence rates.
Panel (b): Microscopic Image of HIV Virus and Immune Cell
This panel is a color-enhanced microscopic image showing HIV particles interacting with a human immune cell.
- A large blue structure represents a human immune cell, likely a T lymphocyte.
- Pink, irregular structures extend from the cell surface and represent portions of the cell membrane and membrane projections.
- Numerous small green spherical particles surrounding the cell represent HIV virions.
The image illustrates HIV particles attaching to and interacting with immune cells, an important step in viral infection. HIV targets immune system cells and uses them to reproduce, ultimately impairing the body's ability to fight infections. Together, the two panels emphasize both the global impact of HIV/AIDS and the cellular interactions that occur during HIV infection.
Figure 2.1.1: Major Components and Functions of the Lymphatic System
This image illustrates the major structures of the human lymphatic system and includes three enlarged views showing the thymus, the formation of lymph, and the internal structure of a lymph node.
Main Body: Lymphatic System Overview
The central image shows a full-body view of the lymphatic system. A network of lymphatic vessels extends throughout the body from the head to the feet. Small lymph nodes are distributed along these vessels, particularly in the neck, armpits, chest, abdomen, and groin.
Several major lymphatic organs are identified:
- The adenoids are located at the back of the nasal cavity in the upper throat.
- The tonsils are located at the back of the mouth and throat.
- The thymus is located in the upper chest, directly above the heart and behind the sternum.
- The spleen is located in the upper left side of the abdomen beneath the rib cage.
- Bone marrow is shown within a long bone of the leg, illustrating the location where many blood and immune cells are produced.
- The right lymphatic duct is shown emptying lymph into a large vein near the base of the neck, where lymph re-enters the bloodstream.
The figure emphasizes that lymphatic vessels collect fluid from tissues throughout the body and return it to the circulatory system.
Enlarged View: Thymus
An enlarged image of the thymus is shown adjacent to the body. This view highlights the thymus as a lobed organ located in the upper chest. The thymus is a primary lymphatic organ where T lymphocytes mature before entering circulation and participating in immune responses.
Enlarged View: Formation and Movement of Lymph
A circular magnified view shows the relationship between tissue cells, blood capillaries, interstitial fluid, lymphatic capillaries, and lymphatic vessels.
Blood capillaries are located among body tissues and release fluid into the spaces surrounding tissue cells. This fluid becomes interstitial fluid, which bathes and nourishes the cells. Excess interstitial fluid enters nearby lymphatic capillaries, where it is then called lymph. The lymph is collected into larger lymphatic vessels and transported through the lymphatic system before eventually returning to the bloodstream.
This view illustrates the pathway:
Blood capillaries → interstitial fluid surrounding tissue cells → lymphatic capillaries → lymphatic vessels
Enlarged View: Lymph Node
A second enlarged view shows a cross-section of a lymph node connected to lymphatic vessels.
The lymph node contains dense collections of lymphocytes and macrophages, concentrated within the interior of the node. These immune cells monitor and filter lymph as it passes through the node, helping remove pathogens, abnormal cells, and foreign material.
This view emphasizes the immune function of lymph nodes as filtration and surveillance sites within the lymphatic system.
The figure demonstrates how the lymphatic system collects excess fluid from body tissues, transports that fluid through lymphatic vessels and lymph nodes, and ultimately returns it to the bloodstream. It also highlights several major lymphatic organs, including the adenoids, tonsils, thymus, spleen, and bone marrow, which contribute to immune system function and the production, maturation, or storage of immune cells. Unlike the cardiovascular system, the lymphatic system does not have a central pump; lymph movement depends on body movement, skeletal muscle contraction, breathing, and one-way valves that prevent backflow and help direct lymph toward the veins of the neck.
Figure 2.1.2: Formation of Lymph and Entry into Lymphatic Capillaries
This image illustrates how interstitial fluid is collected by lymphatic capillaries and becomes lymph. The figure consists of a tissue-level view and an enlarged microscopic view of a lymphatic capillary wall.
Tissue-Level View
The left portion of the figure shows tissue spaces located between body cells. An arteriole supplies blood to a network of blood capillaries within the tissue, and a venule collects blood leaving the capillary bed.
As blood passes through the capillaries, some fluid leaves the bloodstream and enters the spaces between tissue cells. This fluid is called interstitial fluid or tissue fluid. The interstitial fluid surrounds and bathes the tissue cells, providing nutrients and removing wastes.
Interspersed throughout the tissue spaces are branching lymphatic capillaries, which collect excess interstitial fluid. These capillaries merge into larger lymphatic vessels, which transport the collected fluid through the lymphatic system toward the bloodstream.
This portion of the figure demonstrates the pathway:
Blood capillaries → interstitial fluid surrounding tissue cells → lymphatic capillaries → lymphatic vessels
Enlarged View of a Lymphatic Capillary
The enlarged view shows the wall of a lymphatic capillary and the mechanism by which interstitial fluid enters the lymphatic system.
The lymphatic capillary is located among tissue cells and is surrounded by interstitial fluid. The wall of the capillary is composed of overlapping lymph vessel endothelial cells that form flexible endothelial flaps.
Collagen fibers anchor the lymphatic capillary to the surrounding tissue. These fibers help prevent collapse of the capillary and assist in opening the endothelial flaps when tissue pressure rises.
Excess interstitial fluid moves from the spaces between tissue cells through openings between the endothelial flaps and enters the lymphatic capillary. Once the fluid enters the capillary, it is called lymph.
Within the lymphatic capillary, the overlapping endothelial flaps function as one-way entry points. The structure identified as a backflow prevention valve helps prevent lymph from moving back into the surrounding tissues, ensuring that lymph continues to move in one direction through the lymphatic system.
The figure demonstrates how excess fluid that leaves blood capillaries is collected from body tissues and returned to circulation through the lymphatic system. Interstitial fluid becomes lymph after entering lymphatic capillaries through specialized endothelial openings. Collagen fibers, endothelial flaps, and one-way valves help ensure efficient fluid collection and directional movement of lymph from tissues into larger lymphatic vessels.
Figure 2.1.3: Major Trunks and Ducts of the Lymphatic System
This image illustrates how lymph from different regions of the body is collected and returned to the bloodstream through the two major lymphatic drainage pathways: the right lymphatic duct and the thoracic duct.
Main Body: Lymphatic Drainage Regions
The central figure shows a human body divided into two drainage territories.
The right lymphatic duct drains lymph from:
- The right side of the head and neck
- The right upper limb
- The right side of the thorax
The remaining regions of the body drain into the thoracic duct, including:
- The left side of the head and neck
- The left upper limb
- The left side of the thorax
- The abdomen
- The pelvis
- Both lower limbs
The thoracic duct begins in the abdomen at an enlarged sac-like structure called the cisterna chyli, which collects lymph from the lower body before the lymph travels superiorly through the thoracic duct toward the neck.
Right Lymphatic Duct
An enlarged view of the right side of the neck shows the right lymphatic duct near the junction of the right internal jugular vein and the right subclavian vein.
The right internal jugular vein descends from the head and neck, while the right subclavian vein drains blood from the right upper limb. The right lymphatic duct empties lymph into the bloodstream where these veins join, allowing lymph collected from the upper right quadrant of the body to re-enter circulation.
Thoracic Duct
A second enlarged view shows the termination of the thoracic duct on the left side of the neck.
The thoracic duct ascends through the thorax and empties lymph into the venous circulation near the junction of the left internal jugular vein and the left subclavian vein. The left internal jugular vein drains blood from the head and neck, and the left subclavian vein drains blood from the left upper limb.
Through this connection, lymph collected from most of the body is returned to the bloodstream.
The figure demonstrates that lymph collected from tissues throughout the body is ultimately returned to the venous circulation through one of two major lymphatic ducts. The right lymphatic duct drains only the upper right portion of the body, whereas the thoracic duct drains the remainder of the body. The cisterna chyli serves as a collection reservoir for lymph from the lower body before it enters the thoracic duct and is transported to the veins of the neck.
Figure 2.1.4: Hematopoietic System of the Bone Marrow
This image shows hematopoiesis, the process by which blood cells develop from a multipotent hematopoietic stem cell, also called a hemocytoblast. At the top, the multipotent hematopoietic stem cell is shown dividing. One note explains that after division, some cells remain stem cells. Another note explains that the remaining cell follows one of two developmental paths depending on the chemical signals received. These two major pathways are:
- Myeloid stem cell pathway - The myeloid stem cell gives rise to four precursor cell types:
- Megakaryoblast
- Proerythroblast
- Myeloblast
- Monoblast
These develop as follows:
- Megakaryoblast → Megakaryocyte → Platelets
- Proerythroblast → Reticulocyte → Erythrocyte
- Myeloblast → Basophil
- Myeloblast → Neutrophil
- Myeloblast → Eosinophil
- Monoblast → Monocyte → Macrophage
- Lymphoid stem cell pathway - The lymphoid stem cell develops into a lymphoblast. The lymphoblast gives rise to:
- Natural killer cell, also labeled large granular lymphocyte
- Small lymphocyte
The small lymphocyte then develops into:
- T lymphocyte
- B lymphocyte → Plasma cell
Figure 2.1.5: Bone Marrow
This image shows a cross-section of bone marrow.
The outer edge forms a denser, lighter-colored ring that represents compact bone. Inside this outer layer is a porous, lattice-like region that represents spongy bone. Near the center is a lighter-colored area that may represent marrow or internal bone tissue.
The image emphasizes the structural contrast between the solid outer compact bone and the more open, trabecular interior of spongy bone. A small scale bar appears in the upper left, indicating magnification or size reference.
Figure 2.1.6: Location, Structure, and Histology of the Thymus
This image shows the location and internal structure of the thymus within the lymphatic system. On the left, a body-wide lymphatic system diagram includes labeled structures such as adenoid, tonsil, right lymphatic duct entering vein, thymus, heart, spleen, and lymph nodes. A highlighted box in the upper chest marks the thymus, and a large arrow points from this region to enlarged views on the right. The upper right panel shows a tissue view of the thymus. Labels identify:
- medulla
- cortex
- trabeculae
- fibrous capsule
This panel emphasizes the outer fibrous capsule, the internal trabeculae extending inward, and the division between the cortex and medulla. A curved arrow leads from this tissue view to a lower right schematic showing a more detailed internal organization of the thymus. The lower right panel labels:
- fibrous capsule
- cortex
- medulla
- trabecula
- cortical epithelial cell
- thymocytes
- dendritic cell
- macrophage
- blood vessel
- medullary epithelial cell
This detailed view shows the thymus as a layered structure. The outer fibrous capsule surrounds the cortex. Below the cortex is the medulla. Trabeculae extend inward from the capsule. The cortex contains many thymocytes and cortical epithelial cells. The medulla contains medullary epithelial cells, dendritic cells, macrophages, and blood vessels.
Figure 2.1.7: Structure and Histology of a Lymph Node
This image shows the structure of a lymph node using two linked views: a schematic cross-section on the right and a magnified tissue image on the left.
On the right, the lymph node cross-section is labeled with the following structures:
- connective tissue capsule
- subcapsular sinus
- cortex
- trabeculae
- germinal centers
- afferent lymphatic vessels
- efferent lymphatic vessels
The connective tissue capsule forms the outer covering of the lymph node. Just beneath it is the subcapsular sinus. The cortex lies below the capsule and contains germinal centers. Trabeculae extend inward from the capsule into the node. Multiple afferent lymphatic vessels enter the lymph node, while efferent lymphatic vessels leave it. A large arrow points from the schematic view to the tissue image on the left, indicating that the left panel is a magnified view of part of the lymph node.
On the left, the tissue image labels:
- connective tissue capsule
- subcapsular sinus
- cortex
The tissue image also highlights germinal centers within the cortex. An inset image near the top provides an additional magnified view of one of these germinal centers.
Figure 2.1.8: Anatomy and Histology of the Spleen
This image illustrates the anatomical location, internal organization, and microscopic structure of the spleen. The figure consists of two panels: an anatomical cross-section of the spleen and a magnified histological view of splenic tissue.
Panel A: Cross Section of the Spleen
A body reference image shows the spleen located in the upper left region of the abdomen, beneath the diaphragm and protected by the lower rib cage. The enlarged anatomical view shows the spleen adjacent to the diaphragm.
The hilum is located on the medial surface of the spleen and serves as the entry and exit point for blood vessels. The splenic artery enters the spleen through the hilum and supplies oxygenated blood, while the splenic vein exits through the hilum and carries blood away from the organ.
An internal cross-sectional view of the spleen shows two major tissue regions:
- White pulp, which consists of dense lymphatic tissue organized around small arteries and is involved in immune surveillance and immune responses.
- Red pulp, which occupies most of the spleen and is responsible for filtering blood, removing aged or damaged red blood cells, and storing blood components.
Fibrous trabeculae extend inward from the capsule of the spleen, providing structural support and carrying blood vessels through the organ.
Within the splenic tissue, small arterioles deliver blood into the spleen, while venules collect blood that has passed through the organ.
Panel B: Magnified Spleen Histology
The lower panel provides a microscopic view of splenic tissue, illustrating the detailed organization of the white pulp and red pulp.
A central artery (arteriole) runs through the white pulp region. Surrounding the central artery is a germinal center, which contains proliferating lymphocytes involved in immune responses. Encircling the germinal center is the marginal zone, a transition area where blood-borne antigens encounter immune cells.
The surrounding red pulp occupies most of the tissue and contains networks of blood-filled spaces and immune cells. Within the red pulp are venous sinuses, which collect and transport filtered blood, and arterial capillaries, which distribute blood throughout the splenic tissue.
A trabecula is visible extending through the tissue, providing structural support and serving as a pathway for blood vessels.
The figure demonstrates the relationship between the gross anatomy and microscopic organization of the spleen. The spleen receives blood through the splenic artery, filters that blood through the white pulp and red pulp, supports immune responses through lymphocyte-rich regions of the white pulp, removes aged or damaged blood cells within the red pulp, and returns filtered blood to circulation through venous pathways and the splenic vein.
Figure 2.1.9: Locations and Histology of the Tonsils
This image shows the anatomical locations of the major tonsils and the microscopic structure of a palatine tonsil. The figure is divided into two panels.
Panel A: Locations of the Tonsils
The upper portion of the figure illustrates the locations of the pharyngeal, palatine, and lingual tonsils within the head and throat.
A sagittal section of the head and neck shows the palatine tonsil located on each side of the oropharynx, between the oral cavity and the throat. Nearby anatomical structures include:
- The palatine bone, which forms part of the roof of the mouth and separates the oral and nasal cavities.
- The tongue, located on the floor of the oral cavity anterior to the pharynx.
- The mandible, which forms the lower jaw and supports the lower teeth.
- The hyoid bone, located inferior to the tongue and superior to the larynx.
- The trachea, located anteriorly and carrying air toward the lungs.
- The esophagus, located posterior to the trachea and carrying food toward the stomach.
An enlarged view of the upper pharynx shows the pharyngeal tonsil located in the roof and posterior wall of the nasopharynx, behind the nasal cavity. Surrounding structures include:
- The brain, located superior to the nasopharynx.
- The sphenoidal sinus, located within the sphenoid bone above the nasopharynx.
- The sphenoid bone, located at the base of the skull.
A second enlarged view compares the positions of the palatine tonsil and lingual tonsil within the throat. The palatine tonsil is located along the lateral walls of the oropharynx, whereas the lingual tonsil is located at the base of the tongue. The epiglottis is positioned posterior to the tongue and superior to the larynx.
A clinical photograph shows the visible structures of the oral cavity. The hard palate forms the anterior roof of the mouth, while the soft palate forms the posterior roof. The uvula hangs from the posterior edge of the soft palate. The palatine tonsils, shown enlarged because of infection, are located on either side of the back of the throat. The tongue occupies the floor of the oral cavity.
Panel B: Histology of the Palatine Tonsil
The lower panel shows a microscopic view of palatine tonsil tissue.
The outer surface is lined by stratified squamous epithelium, which forms a protective covering exposed to the oral cavity.
Deep folds of the epithelial surface extend inward to form crypts. These crypts increase the surface area of the tonsil and help trap microorganisms and foreign material that enter through the mouth or throat.
Beneath the epithelium are numerous germinal centers, which are regions of densely packed lymphocytes. These germinal centers are sites of immune-cell proliferation and activation during immune responses.
The figure demonstrates the locations of the major tonsils that form part of the body's first line of immune defense against inhaled or ingested pathogens. The pharyngeal tonsil is located in the nasopharynx, the palatine tonsils are located on either side of the oropharynx, and the lingual tonsil is located at the base of the tongue. The histology of the palatine tonsil shows crypts and germinal centers that increase exposure to foreign material and support immune surveillance and immune responses.
Figure 2.1.10:Mucosa-associated Lymphoid Tissue
This image shows a histological cross-section of intestinal tissue labeled to highlight Peyer’s patches and mucosa.
The section is circular with a central open lumen. Surrounding the lumen is the mucosa, labeled along the inner lining of the intestinal wall. Within the wall are several large, darkly stained oval regions labeled Peyer’s patches. These clustered lymphatic nodules are positioned beneath the mucosal surface.
A small inset in the upper right shows a reduced overview of the same tissue section, providing orientation for the larger labeled image.
Bronchus-associated lymphoid tissue (BALT) consists of lymphoid follicular structures with an overlying epithelial layer found along the bifurcations of the bronchi, and between bronchi and arteries. They also have the typically less-organized structure of other lymphoid nodules. These tissues, in addition to the tonsils, are effective against inhaled pathogens.
Figure 2.2.1: Cooperation between Innate and Adaptive Immune Responses
This image shows how pathogens entering through the upper airway or oral region can encounter both innate immunity and adaptive immunity, with the palatine tonsil highlighted as a site of immune activity. Starting point
- Pathogens are shown entering near the upper airway or oral cavity.
- The palatine tonsil is labeled as one important lymphatic structure in this region.
Innate immunity - Arrows from the entry region point to the section labeled Innate Immunity, which is divided into surface defenses and internal defenses.
- Surface defenses structures act as physical or chemical barriers that help block or trap pathogens before they enter deeper tissues:
- Skin
- Hair
- Mucus
- Internal defenses - A label for histamine appears near the internal defense panel, indicating inflammatory signaling involved in innate immune responses.
- Mast cells and basophils, associated with the inflammatory response
- Natural killer cells
- Complement system
- Phagocytes:
- Monocytes
- Neutrophils
- Macrophages
Adaptive immunity - Another arrow leads to the section labeled Adaptive Immunity, shown in the germinal center of the palatine tonsil. Key components listed:
- T lymphocyte
- Antigen-presenting cells
- B lymphocytes
Within the germinal center, labels identify:
- T memory cells
- T effector cells
- B memory cells
- B effector cells
- antibodies
This shows that adaptive immunity includes activation and differentiation of lymphocytes, formation of memory cells, and antibody production.
Figure 2.2.2: Complement Cascade and Function
This image shows the complement cascade, beginning when complement protein C1 binds to an antigen–antibody complex on an invading pathogen and ending with formation of the membrane attack complex.
Initiation: An invading pathogen has an antigen on its surface. An antibody binds to the antigen, forming an antigen–antibody complex. Complement protein C1 binds to this complex, triggering complement components C2 and C4 to split.
Formation of C3 convertase: Fragments of C2 and C4 combine to form an enzyme called C3 convertase.
Splitting of C3: C3 convertase splits C3 into two fragments: C3a and C3b. Interaction with additional factors P, B, and D is also indicated.
- C3a attracts phagocytes to the infection site.
- C3b binds to the pathogen surface.
Formation of C5 convertase: A fragment from C3 joins C3 convertase to form C5 convertase. This enzyme splits C5 into C5a and C5b.
Formation of the membrane attack complex: C5b combines with complement proteins C6, C7, C8, and C9 to form the membrane attack complex. This complex creates a pore in the pathogen’s membrane, allowing water to enter and causing the pathogen to lyse.
The splitting of the C3 protein is the common step to both pathways. In the alternate pathway, C3 is activated spontaneously and, after reacting with the molecules factor P, factor B, and factor D, splits apart. The larger fragment, C3b, binds to the surface of the pathogen and C3a, the smaller fragment, diffuses outward from the site of activation and attracts phagocytes to the site of infection. Surface-bound C3b then activates the rest of the cascade, with the last five proteins, C5–C9, forming the membrane-attack complex (MAC). The MAC can kill certain pathogens by disrupting their osmotic balance. The MAC is especially effective against a broad range of bacteria. The classical pathway is similar, except the early stages of activation require the presence of antibody bound to antigen, and thus is dependent on the adaptive immune response. The earlier fragments of the cascade also have important functions. Phagocytic cells such as macrophages and neutrophils are attracted to an infection site by chemotactic attraction to smaller complement fragments. Additionally, once they arrive, their receptors for surface-bound C3b opsonize the pathogen for phagocytosis and destruction.
Figure 2.2.3: Inflammatory Response
This image shows two stages of the inflammatory response after tissue injury and pathogen entry.
- Detection and histamine release is the first stage which shows the signal that inflammation starts.
- Mast cells detect injury in nearby tissue.
- In response, they release histamine.
- Pathogens are shown at the wound site.
- Histamine initiates the inflammatory response.
- Increased blood flow and immune cell response is the second stage which shows how inflammation recruits immune defenses to the injured tissue.
- Histamine increases blood flow to the wound site.
- This brings phagocytes and other immune cells into the area.
- Phagocytes move toward the pathogens and help neutralize them.
- Visible effects of inflammation - The increased blood flow causes the wound area to:
- swell
- redden
- become warm
- become painful
This reaction also brings in the cells of the innate immune system, allowing them to get rid of the sources of a possible infection. Inflammation is part of a very basic form of immune response. The process not only brings fluid and cells into the site to destroy the pathogen and remove it and debris from the site, but also helps to isolate the site, limiting the spread of the pathogen. Acute inflammation is a short-term inflammatory response to an insult to the body. If the cause of the inflammation is not resolved, however, it can lead to chronic inflammation, which is associated with major tissue destruction and fibrosis. Chronic inflammation is ongoing inflammation. It can be caused by foreign bodies, persistent pathogens, and autoimmune diseases such as rheumatoid arthritis.
Figure 2.3.1: Alpha-beta T Cell Receptor
This image shows the structure of a T-cell receptor embedded in a cell membrane.
- Main receptor chains are made of two protein chains. These two chains are positioned side by side and together form the receptor.
- alpha chain
- beta chain
- Variable region
- The top portion of the receptor is labeled variable region.
- This region is the part involved in recognizing specific antigens.
- Constant region
- Below the variable region is the constant region.
- This portion provides structural support and remains more similar across receptors of the same type.
- Transmembrane region
- The lower part of the receptor passes through the cell membrane.
- This portion is labeled transmembrane region.
- It anchors the receptor in the membrane.
- Membrane
- The receptor is shown extending through a phospholipid bilayer.
- This indicates that the T-cell receptor is attached to the cell surface.
Figure 2.3.2: Antigenic Determinants
This image shows a protein with multiple antigenic determinants interacting with three different T cells.
- Central protein
- A protein is shown in the center as a folded ribbon structure.
- This protein contains multiple labeled antigenic determinants.
- Antigenic determinants
- Three separate antigenic determinants are labeled on different parts of the same protein.
- These represent distinct regions of the protein that can be recognized by immune cells.
- T cell 1
- T cell 1 is shown on the left.
- Its receptor is positioned to recognize one antigenic determinant on the protein.
- T cell 2
- T cell 2 is shown at the bottom.
- Its receptor is positioned to recognize a different antigenic determinant on the same protein.
- T cell 3
- T cell 3 is shown on the right.
- Its receptor is positioned to recognize another antigenic determinant on the protein.
Figure 2.3.3: Antigen Processing and Presentation by a Dendritic Cell
This image sh ows how a dendritic cell pr ocesses an external pathogen and presents antigen to a T cell using MHC proteins.
- Step 1: Pathogen uptake
- A pathogen or extracellular antigen is taken into the dendritic cell by phagocytosis.
- The material is enclosed in a vesicle.
- A lysosome releases digestive enzymes that break down the pathogen and extract antigen fragments.
- Step 2: Antigen binding to MHC proteins
- Antigen fragments from the digested pathogen enter vesicles inside the dendritic cell.
- MHC proteins enter these vesicles and bind the antigen fragments.
- The diagram labels:
- MHC I protein
- MHC II protein
- peptide-binding cleft
- antigen from digested pathogen
- Step 3: Transport to the cell surface
- The MHC proteins, now carrying antigen fragments, leave the vesicle.
- They move to the outer surface of the dendritic cell membrane.
- Step 4: Antigen presentation
- At the cell surface, the dendritic cell presents antigen fragments on MHC proteins.
- A T cell receptor on a nearby T cell binds to the antigen-MHC complex.
- This interaction activates T cells that recognize the displayed antigen.
Figure 2.3.4: T-Cell Development and Selection in the Thymus
This image illustrates the development and selection of T lymphocytes in the thymus, beginning with untrained thymocytes from the bone marrow and ending with mature helper and cytotoxic T cells that are released to the lymphatic system. The process is organized into five numbered steps and occurs as cells move from the thymic cortex to the medulla.
Step 1
Untrained (−−) thymocytes from bone marrow enter the thymic cortex.
The process begins with immature thymocytes that originate in the bone marrow. These cells enter the cortex of the thymus and are identified as CD4− CD8−, meaning they express neither the CD4 receptor nor the CD8 receptor.
Step 2
Thymic epithelial cells present MHC proteins to the untrained thymocytes. Thymocytes that successfully bind with the MHC proteins continue while those that cannot undergo apoptosis. This is positive selection (selecting those that bind).
In the cortex of the thymus, thymic epithelial cells display MHC proteins. The figure shows an MHC molecule on a thymic epithelial cell interacting with an immature thymocyte receptor.
- If the immature thymocyte receptor successfully binds the MHC protein, the thymocyte survives.
- If the MHC protein does not bind the thymocyte receptor, the thymocyte undergoes apoptosis and is eliminated.
This process is called positive selection because cells capable of recognizing self-MHC molecules are selected to survive.
Step 3
Thymocytes that survive positive selection become double positive (+ +) because they receive both a CD4 receptor and a CD8 receptor.
The surviving thymocytes now express both CD4 and CD8 receptors and are identified as CD4+ CD8+. The figure shows both receptors on the cell surface as the thymocytes move from the cortex toward the medulla of the thymus.
Step 4
The surviving thymocytes move to the thymic medulla where they encounter antigen-presenting cells (APCs). These APCs present self-antigens from other body cells. Thymocytes that bind with the self-antigens undergo apoptosis, as this indicates that they will attack body cells. This is called negative selection (selection for cells that don't bind).
In the medulla of the thymus, dendritic cells functioning as antigen-presenting cells display self-antigens derived from body tissues.
The figure shows two possible outcomes:
- If neither the CD4 receptor nor the CD8 receptor binds the self-antigen, the thymocyte survives.
- If either the CD4 receptor or the CD8 receptor binds the self-antigen, the thymocyte undergoes apoptosis.
This process is known as negative selection because self-reactive cells are eliminated, promoting self-tolerance and helping prevent autoimmunity.
Step 5
Cell signals cause the self-tolerant thymocytes to express either the CD4 or the CD8 receptor, but not both. Those that express the CD4 receptor become helper T cells (TH) while those that express the CD8 receptor become cytotoxic T cells (TC).
The surviving self-tolerant thymocytes lose one of the two receptors and become single-positive cells:
- CD4+ CD8− thymocytes differentiate into mature helper T cells (TH).
- CD4− CD8+ thymocytes differentiate into mature cytotoxic T cells (TC).
After maturation, these cells leave the thymus and enter the lymphatic system, where they circulate and participate in adaptive immune responses.
The figure demonstrates how developing T cells are selected for two critical properties. Through positive selection in the thymic cortex, T cells must be able to recognize the body's own MHC molecules. Through negative selection in the medulla, T cells that react strongly to self-antigens are eliminated. The remaining self-tolerant T cells mature into either helper T cells or cytotoxic T cells and are released into the lymphatic system to participate in immune defense.
Figure 2.3.5: Clonal Selection and Expansion of T Lymphocytes
This image shows activation of a naïve cytotoxic T cell by an antigen-presenting cell and the two main outcomes of that activation.
- Activation of the naïve cytotoxic T cell - shows how a cytotoxic T cell is activated by recognition of a specific antigen presented on MHC class I.
- A naïve TC cell is shown at the top.
- An antigen-presenting cell, identified as a dendritic cell, displays an antigen fragment on MHC class I.
- The naïve cytotoxic T cell binds to this antigen-MHC class I complex through its T cell receptor and CD8.
- After binding, the cell becomes an activated TC cell.
- Clonal expansion and effector function - represents production of multiple effector cytotoxic T cells that respond to infected target cells.
- One pathway from the activated TC cell shows that activated cytotoxic T cells are cloned.
- These cloned cells destroy infected cells in the body.
- Memory cell formation - represents immunological memory and a faster response during future exposure to the same antigen.
- A second pathway shows that memory TC cells are produced.
- These memory cells are activated if the same antigen is encountered again.
Figure 2.3.6: Pathogen Presentation
This image compares helper T-cell activation and cytotoxic T-cell activation and shows the different responses each cell type produces.
- Helper T-cell pathway - The cytokines activate much of the adaptive and nonadaptive immune system during infection.
- An antigen-presenting cell, identified as a dendritic cell, displays an antigen on MHC II.
- An activated T helper cell (TH cell) binds to this antigen-MHC II complex through its T cell receptor and CD4.
- After activation, the helper T cell releases cytokines.
- Cytotoxic T-cell pathway - These enzymes and proteins damage the infected cell membrane and contribute to destruction of the infected cell.
- An infected cell displays antigens on MHC I.
- An activated cytotoxic T cell (TC cell) binds to this antigen-MHC I complex through its T cell receptor and CD8.
- After activation, the cytotoxic T cell releases granzymes and perforins.
Although the correlation is not 100 percent, CD4-bearing T cells are associated with helper functions and CD8-bearing T cells are associated with cytotoxicity. These functional distinctions based on CD4 and CD8 markers are useful in defining the function of each type.
Figure 2.4.1: Antibody and IgG2 Structures
This image is a two-panel antibody image showing a labeled structure diagram and a 3D antibody model.
Panel (a) - This panel shows a simplified diagram of an antibody shaped like the letter Y. Labeled antibody structure diagram:
- The top arms of the Y are labeled antigen-binding sites, where the antibody attaches to foreign substances.
- These upper portions are called the variable regions, which can differ in shape to bind to different antigens.
- The lower stem is labeled the constant region, which has a more stable structure.
- The antibody is made of two types of protein chains:
- Heavy chains, which form the inner and longer parts of the structure
- Light chains, which are shorter and attached to the outer sides
- The chains are connected by disulfide bonds, shown as links between segments.
- The lower stem is also labeled the Fc region, which helps activate immune system responses.
Panel (b) - This panel shows a three-dimensional ribbon model of an antibody protein. 3D antibody structure model:
- The structure keeps the same general Y shape shown in the diagram.
- Different colors distinguish sections of the protein chains.
- The folded ribbon form shows how the protein is arranged in three-dimensional space.
- The two upper arms correspond to the antigen-binding regions.
- The lower portion corresponds to the constant region.
Figure 2.4.2: The Five Immunoglobulin (Ig) Classes
This image compares the five major classes of immunoglobulins (antibodies): IgM, IgG, Secretory IgA, IgE, and IgD. The figure presents both the molecular structure of each antibody class and a comparison of their major characteristics and functions.
At the top of the figure, each antibody class is represented by a simplified structural diagram.
- IgM is shown as a pentamer, consisting of five antibody units joined together in a circular arrangement.
- IgG is shown as a monomer, consisting of a single Y-shaped antibody unit.
- Secretory IgA is shown as a dimer, consisting of two joined antibody units connected by a secretory component.
- IgE is shown as a monomer, consisting of a single Y-shaped antibody unit.
- IgD is shown as a monomer, consisting of a single Y-shaped antibody unit.
The figure compares the five antibody classes using the following characteristics.
IgM (Pentamer)
- Heavy chain: μ (mu)
- Number of antigen-binding sites: 10
- Molecular weight: 900,000 daltons
- Percentage of total antibody in serum: 6%
- Crosses placenta: No
- Fixes complement: Yes
- Fc region binds to: None Shown
- Function:
- Main antibody of the primary immune response
- Most effective antibody for complement activation
- Monomer form of IgM functions as a B-cell receptor
IgG (Monomer)
- Heavy chain: γ (gamma)
- Number of antigen-binding sites: 2
- Molecular weight: 150,000 daltons
- Percentage of total antibody in serum: 80%
- Crosses placenta: Yes
- Fixes complement: Yes
- Fc region binds to: Phagocytes
- Function:
- Main antibody of secondary immune responses
- Neutralizes toxins
- Promotes phagocytosis through opsonization
Secretory IgA (Dimer)
- Heavy chain: α (alpha)
- Number of antigen-binding sites: 4
- Molecular weight: 385,000 daltons
- Percentage of total antibody in serum: 13%
- Crosses placenta: No
- Fixes complement: No
- Fc region binds to: None Shown
- Function:
- Secreted into mucus, tears, saliva, and colostrum
- Provides protection at mucosal surfaces and in body secretions
IgE (Monomer)
- Heavy chain: ε (epsilon)
- Number of antigen-binding sites: 2
- Molecular weight: 200,000 daltons
- Percentage of total antibody in serum: 0.002%
- Crosses placenta: No
- Fixes complement: No
- Fc region binds to: Mast cells and basophils
- Function:
- Antibody involved in allergic reactions
- Participates in defense against parasitic infections
IgD (Monomer)
- Heavy chain: δ (delta)
- Number of antigen-binding sites: 2
- Molecular weight: 180,000 daltons
- Percentage of total antibody in serum: 1%
- Crosses placenta: No
- Fixes complement: No
- Fc region binds to: None Shown
- Function:
- Functions as a B-cell receptor
The figure demonstrates that the five immunoglobulin classes differ in structure, abundance, and function. IgG is the most abundant antibody in serum and is the only class shown crossing the placenta. IgM has the greatest number of antigen-binding sites and is the strongest activator of complement. Secretory IgA is specialized for protection of mucosal surfaces and body secretions. IgE is associated with allergic responses and antiparasitic immunity, while IgD primarily functions as a receptor on B lymphocytes.
Figure 2.4.3: Clonal Selection of B Cells
This image compares the primary immune response (first exposure to an antigen) and the secondary immune response (later exposure to the same antigen).
Left Side - Primary Response (First Exposure):
- Small particles labeled antigens enter the body.
- A B cell recognizes and binds to the antigen using receptors on its surface.
- The B cell becomes an activated B cell.
- The activated B cell undergoes clonal expansion, meaning it makes many identical copies of itself.
These copies develop into two types of cells:
- Plasma cells
- These cells produce and release antibodies (shown as small Y-shaped molecules).
- Antibody production is relatively slow during the first exposure.
- Memory B cells
- These cells remain in the body long after the infection.
- They “remember” the specific antigen for future responses.
Right Side - Secondary Response (Second Exposure):
- When the same antigen enters the body again, memory B cells quickly recognize it.
- Memory B cells rapidly form a clone of cells, much faster than during the primary response.
These cells again differentiate into:
- Plasma cells
- They produce large amounts of antibodies very quickly.
- Memory B cells
- They are replenished to maintain long-term immunity.
Figure 2.4.4: Primary and Secondary Antibody Responses
This image is a graph comparing the primary immune response and the secondary immune response.
Axes (What the graph shows):
- The horizontal axis (x-axis) represents time in weeks.
- The vertical axis (y-axis) represents the concentration of antibodies in the blood.
- A red curve shows how antibody levels change over time.
Primary Response (First Exposure):
- The graph begins with an initial exposure to an antigen (a foreign substance).
- There is a delay (lag phase) before antibodies start to appear.
- Antibody levels then increase slowly, forming a small peak.
- After reaching this peak, antibody levels gradually decrease.
This response is slow and relatively weak because the immune system is encountering the antigen for the first time and must learn how to respond.
Secondary Response (Second Exposure):
- Later on the graph, there is a second exposure to the same antigen.
- This time, antibody levels rise much more quickly, with little or no delay.
- The graph shows a much higher peak, meaning many more antibodies are produced.
- The response is also longer-lasting compared to the primary response.
This happens because memory cells for med during the first exposure allow the immune system to respond faster and more effectively
Figure 2.4.5: T and B Cell Binding
This image shows the activation of a B cell, including how it recognizes an antigen and receives help from a helper T cell.
Step 1: Antigen Recognition by B Cell
- On the left, a B cell is shown with B cell receptors on its surface.
- Small particles labeled antigens bind to these receptors.
- This step represents the B cell recognizing a foreign substance.
Step 2: Antigen Processing and Presentation
- After binding the antigen, the B cell processes it internally.
- The B cell then displays a piece of the antigen on its surface using a molecule called MHC class II (MHC II).
Step 3: Interaction with Helper T Cell
- On the right, a helper T cell is shown interacting with the B cell.
- The helper T cell uses its T cell receptor to recognize the antigen presented on MHC II.
- The helper T cell also uses a surface molecule called CD4 to stabilize this interaction.
Step 4: Activation Through Cytokines
- The helper T cell releases cytokines (chemical signaling molecules).
- These cytokines send signals that activate the B cell.
Step 5: Activated B Cell
- The B cell is now labeled as an activated B cell.
- Once activated, the B cell can divide and later develop into:
- Plasma cells, which produce antibodies
- Memory B cells, which help respond faster in future infections
Figure 2.5.1: HIV Disease Progression Seroconversion
This image is a graph showing how HIV virus concentration and anti-HIV antibody levels change over time in the blood.
- Axes
- The horizontal axis (x-axis) represents time, starting with months and continuing into years.
- The vertical axis (y-axis) represents the concentration in blood, meaning how much virus or antibody is present.
- Two lines are shown:
- One represents HIV virus levels
- The other represents anti-HIV antibodies
- Early Stage (Initial Infection)
- Soon after infection, the virus level rises very quickly to a high peak.
- At this point, antibody levels are low because the immune system is just starting to respond.
- As time progresses, antibody levels increase, which causes the virus level to drop sharply.
- Middle Stage (Chronic Phase)
- During the following months and years, the virus remains at a low but steady level.
- Antibody levels remain relatively high and stable.
- This stage represents a long period where the infection is present but partially controlled by the immune system.
- Late Stage (Disease Progression)
- After several years, the graph shows the virus level rising again.
- At the same time, antibody levels begin to decline.
- This indicates that the immune system is weakening and is less able to control the infection.
Figure 2.5.2: IgA Immunity
This image shows how the immune system in the intestine responds to antigens and produces secretory IgA antibodies for protection.
Top Section: Intestinal Surface
- The upper part shows a lining of epithelial cells forming the intestinal wall.
- A layer of mucus covers these cells.
- Specialized cells called M cells take in antigens (small foreign particles) from the intestinal lumen and transport them across the epithelial layer.
Left Side: Peyer’s Patch (Immune Activation Area)
- Beneath the epithelial layer is a region labeled Peyer’s patch, which contains organized lymphoid follicles.
- Inside this region are:
- B cells
- T cells
- Dendritic cells, which present antigens to T cells using MHC class II molecules
- B cells use their B cell receptors to recognize antigens.
- With help from T cells, B cells become activated.
Middle Section: Lymphatic System
- Activated immune cells move through the lymphatic system, shown as arrows leading away from the Peyer’s patch.
- This step represents the circulation and distribution of immune cells.
Right Side: Antibody Production
- Activated B cells differentiate into plasma cells.
- Plasma cells produce IgA antibodies.
- These antibodies are transported back toward the epithelial surface.
Top Right: Secretion into Mucus
- Secretory IgA antibodies are released into the mucus layer.
- These antibodies bind to antigens and help prevent pathogens from attaching to or invading epithelial cells.
Figure 2.6.1: Immune Hypersensitivity
The figure compares the four major types of hypersensitivity reactions: Type I (IgE-mediated hypersensitivity), Type II (IgG-mediated cytotoxic hypersensitivity), Type III (immune complex-mediated hypersensitivity), and Type IV (cell-mediated hypersensitivity). Each column illustrates the immune mechanism responsible for tissue damage and provides representative disorders or conditions associated with that reaction type.
Type I: IgE-Mediated Hypersensitivity
An allergen binds to allergen-specific IgE antibodies attached to the surface of a mast cell through Fc receptors. Crosslinking of the IgE antibodies triggers mast-cell degranulation, resulting in the release of inflammatory mediators.
The figure states: IgE is bound to mast cells via its Fc portion. When an allergen binds to these antibodies, crosslinking of IgE induces degranulation.
Examples shown include localized and systemic anaphylaxis, seasonal allergies including hay fever, food allergies such as shellfish and peanut allergies, hives, and eczema.
Type II: IgG-Mediated Cytotoxic Hypersensitivity
IgG antibodies bind to antigens located on the surface of a target cell. The figure shows two mechanisms by which the target cell can be damaged.
Antibody-dependent cellular cytotoxicity (ADCC): A cytotoxic cell bearing Fc receptors recognizes antibody-coated target cells and destroys them.
Complement activation: Binding of antibodies to surface antigens activates the complement system, resulting in cell damage.
The figure states: Cells are destroyed by bound antibody, either by activation of complement or by a cytotoxic T cell with an Fc receptor for the antibody (ADCC).
Example shown: Red blood cells destroyed by complement and antibody during a transfusion of mismatched blood type or during erythroblastosis fetalis.
Type III: Immune Complex-Mediated Hypersensitivity
Circulating antigen-antibody complexes, shown as free-floating immune complexes, become deposited in tissues. These deposits activate the complement system and attract neutrophils, resulting in inflammation and tissue injury.
The figure states: Antigen-antibody complexes are deposited in tissues, causing activation of complement, which attracts neutrophils to the site.
Examples shown include glomerulonephritis, rheumatoid arthritis, and systemic lupus erythematosus.
Type IV: Cell-Mediated Hypersensitivity
Unlike the other hypersensitivity types, Type IV reactions do not involve antibodies. A sensitized Th1 cell recognizes antigen and releases cytokines. These cytokines activate macrophages and cytotoxic T cells, leading to inflammation and tissue damage. An activated macrophage is depicted as a major effector cell in the reaction.
The figure states: Th1 cells secrete cytokines, which activate macrophages and cytotoxic T cells and can cause macrophage accumulation at the site.
Examples shown include contact dermatitis, tuberculin reaction, and autoimmune diseases such as diabetes mellitus type I, multiple sclerosis, and rheumatoid arthritis.
The figure compares four distinct mechanisms of hypersensitivity. Type I reactions involve IgE-mediated mast-cell degranulation. Type II reactions involve IgG antibodies that destroy antibody-coated cells through complement activation or ADCC. Type III reactions involve deposition of antigen-antibody complexes in tissues, causing complement activation and neutrophil recruitment. Type IV reactions are mediated by Th1 cells, macrophages, and cytotoxic T cells through cytokine signaling without antibody involvement. Together, the four pathways illustrate the major mechanisms by which immune responses can cause allergic, autoimmune, and inflammatory tissue damage.
Figure 2.6.2: Autoimmune Disorders
This two-panel figure compares characteristic physical effects of autoimmune disorders. Panel (a) focuses on severe joint damage associated with rheumatoid arthritis, while Panel (b) illustrates multiple body systems that may be affected by systemic lupus erythematosus (SLE).
Panel (a): Hand X-Ray Showing Rheumatoid Arthritis
The left panel is an X-ray image of both hands. The bones of the wrists, palms, and fingers are visible. The joints of multiple fingers show significant deformity, including joint narrowing, displacement, and abnormal angulation of the fingers. Several fingers appear bent away from their normal alignment, and the joint spaces are irregular. The changes are most pronounced in the small joints of the hands and fingers.
The image demonstrates the destructive effects of chronic rheumatoid arthritis on synovial joints. Persistent autoimmune inflammation damages cartilage, bone, and supporting connective tissues, leading to pain, loss of joint function, stiffness, and visible deformities of the hands.
Panel (b): Systemic Effects of Systemic Lupus Erythematosus (SLE)
The right panel shows a full-body anatomical illustration highlighting multiple organs and body systems affected by lupus. Labels identify common signs and symptoms throughout the body.
Systemic Effects
- Low-grade fever
- Photosensitivity (increased sensitivity to sunlight)
These symptoms reflect widespread immune activation and inflammation.
Psychological Effects
- Fatigue
- Loss of appetite
These generalized symptoms are common in chronic autoimmune disease and may affect quality of life and daily functioning.
Mouth and Nose
- Ulcers
The figure indicates ulcer formation within the oral or nasal mucosa.
Face
- Butterfly rash
A characteristic butterfly-shaped rash extends across the cheeks and bridge of the nose. This is a common clinical sign of lupus.
Muscles
- Aches
Muscle pain and discomfort may occur due to systemic inflammation.
Joints
- Arthritis
Inflammation of the joints may cause pain, swelling, stiffness, and reduced mobility.
Pleura
- Inflammation
The pleura, the membranes surrounding the lungs, may become inflamed, causing pleuritis and chest discomfort.
Pericardium
- Inflammation
The pericardium, the sac surrounding the heart, may become inflamed, resulting in pericarditis.
Fingers and Toes
- Poor circulation
Blood flow to the extremities may be reduced, resulting in color changes, numbness, or discomfort.
Together, the two panels illustrate that autoimmune diseases can affect the body in different ways. Rheumatoid arthritis primarily targets joints, producing progressive joint destruction and deformity, especially in the hands. Systemic lupus erythematosus affects multiple organ systems throughout the body, producing a wide range of symptoms involving the skin, joints, muscles, circulatory system, respiratory system, cardiovascular system, and mucous membranes. The figure emphasizes that autoimmune disorders result from immune responses directed against the body's own tissues and can cause both localized and systemic disease.
Figure 2.7.1: Rh Incompatibility and Maternal Sensitization During Pregnancy
This image illustrates how Rh incompatibility can develop between an Rh-negative mother and an Rh-positive fetus. The figure consists of three parts: a diagram of the placenta and two enlarged panels showing the first and second exposures to Rh-positive fetal red blood cells.
Placenta Structure
The left side of the figure shows the placenta connecting the fetal and maternal circulations.
The umbilical artery and vein carry blood between the fetus and the placenta. Within the placenta, branches of the fetal circulation are enclosed by the embryonic chorion, a membrane that normally separates fetal blood from maternal blood.
Surrounding the chorion is the maternal blood pool, which receives blood from a placental arteriole (maternal) and drains into a placental venule (maternal). Although nutrients, gases, and wastes are exchanged across the placental barrier, fetal and maternal blood are normally kept separate by the embryonic chorion.
First Exposure: Birth of First Rh⁺ Infant
The upper-right panel illustrates the first exposure of an Rh-negative mother to Rh-positive fetal blood.
The panel identifies:
- Infant blood
- Rh⁺ infant erythrocytes
- Embryonic chorion
- Rh⁻ maternal blood
- Maternal Rh antibody
Step 1: During birth, Rh⁺ fetal erythrocytes leak into maternal blood after breakdown of the embryonic chorion, which normally isolates fetal and maternal blood.
The figure shows fetal red blood cells crossing from the infant circulation into the maternal circulation.
Step 2: Maternal B cells are activated by the Rh antigen and produce large amounts of anti-Rh antibodies.
The figure shows activated maternal B cells releasing antibodies directed against the Rh antigen. Because this antibody production occurs after fetal blood enters the maternal circulation, the first Rh-positive infant is usually not harmed.
Second Exposure: Rh⁺ Fetus
The lower-right panel illustrates a later pregnancy involving another Rh-positive fetus.
The panel identifies:
- Infant blood
- Rh⁺ infant erythrocytes
- Embryonic chorion
- Rh⁻ maternal blood
- Maternal Rh antibody
Step 1: Rh antibody titer in the mother's blood is elevated after the first exposure.
The figure shows numerous anti-Rh antibodies already present within the maternal circulation as a result of immune memory from the first pregnancy.
Step 2: Rh antibodies are small enough to cross the embryonic chorion and attack the fetal erythrocytes.
Unlike fetal red blood cells, maternal antibodies can pass through the placental barrier. The figure shows anti-Rh antibodies crossing the embryonic chorion, binding to Rh-positive fetal erythrocytes, and targeting them for destruction.
The figure demonstrates the development of Rh incompatibility. During the first pregnancy, exposure to Rh-positive fetal erythrocytes sensitizes an Rh-negative mother and stimulates production of anti-Rh antibodies. During a subsequent pregnancy with an Rh-positive fetus, preexisting maternal anti-Rh antibodies cross the placenta and attack fetal red blood cells, potentially causing hemolytic disease of the newborn (erythroblastosis fetalis). The figure emphasizes the role of maternal immune memory and the ability of antibodies, but not fetal red blood cells, to cross the placental barrier.
Figure 2.7.2: Karposi’s Sarcoma Lesions
This image shows a close-up view of human skin with multiple visible lesions.
- The skin surface contains numerous spots and patches of varying sizes.
- The lesions are mostly red to dark purple in color, with some appearing darker in the center.
- Many of the spots are raised and irregular in shape, while others are flatter.
- The lesions are spread unevenly across the skin and appear in clusters.
- Some areas show larger patches where smaller spots have merged together.
- The surrounding skin appears lighter in color, creating contrast with the darker lesions.
This page titled 2.11: Alternate Text Descriptions was last modified on Sat, 26 Sep 2026 20:13:30 GMT and is shared under a CC BY 4.0 license and was authored, remixed, and/or curated by Lakshmikanta Sengupta and Susmita Sengupta.
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