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Chapter 43 The Immune System PowerPoint Lectures for Biology, Seventh Edition Neil Campbell and Jane Reece Lectures by Chris Romero Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • Overview: Reconnaissance, Recognition, and Response • An animal must defend itself – From the many dangerous pathogens it may encounter in the environment • Two major kinds of defense have evolved that counter these threats – Innate immunity and acquired immunity Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • Innate immunity – Is present before any exposure to pathogens and is effective from the time of birth – Involves nonspecific responses to pathogens Figure 43.1 Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings 3m • Acquired immunity, also called adaptive immunity – Develops only after exposure to inducing agents such as microbes, toxins, or other foreign substances – Involves a very specific response to pathogens Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • A summary of innate and acquired immunity INNATE IMMUNITY Rapid responses to a broad range of microbes External defenses Skin Internal defenses Phagocytic cells Mucous membranes Antimicrobial proteins Secretions Inflammatory response Invading microbes (pathogens) Figure 43.2 Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings ACQUIRED IMMUNITY Slower responses to specific microbes Natural killer cells Humoral response (antibodies) Cell-mediated response (cytotoxic lymphocytes) • Concept 43.1: Innate immunity provides broad defenses against infection • A pathogen that successfully breaks through an animal’s external defenses – Soon encounters several innate cellular and chemical mechanisms that impede its attack on the body Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings External Defenses • Intact skin and mucous membranes – Form physical barriers that bar the entry of microorganisms and viruses • Certain cells of the mucous membranes produce mucus – A viscous fluid that traps microbes and other particles Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • In the trachea, ciliated epithelial cells – Sweep mucus and any entrapped microbes upward, preventing the microbes from entering the lungs 10m Figure 43.3 Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • Secretions of the skin and mucous membranes – Provide an environment that is often hostile to microbes • Secretions from the skin – Give the skin a pH between 3 and 5, which is acidic enough to prevent colonization of many microbes – Also include proteins such as lysozyme, an enzyme that digests the cell walls of many bacteria Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Internal Cellular and Chemical Defenses • Internal cellular defenses – Depend mainly on phagocytosis • Phagocytes, types of white blood cells – Ingest invading microorganisms – Initiate the inflammatory response Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Phagocytic Cells • Phagocytes attach to their prey via surface receptors – And engulf them, forming a vacuole that fuses with a lysosome 1 Pseudopodia surround microbes. Microbes 2 Microbes are engulfed into cell. MACROPHAGE 3 Vacuole containing microbes forms. Vacuole Lysosome containing enzymes 4 Vacuole and lysosome fuse. 5 Toxic compounds and lysosomal enzymes destroy microbes. Figure 43.4 Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings 6 Microbial debris is released by exocytosis. Neutrophil (60-70% of all leukocytes) exhibiting phagocytosis Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • Macrophages, a specific type of phagocyte – Can be found migrating through the body – Can be found in various organs of the lymphatic system Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • The lymphatic system – Plays an active role in defending the body from pathogens 1 Interstitial fluid bathing the tissues, along with the white blood cells in it, continually enters lymphatic capillaries. Interstitial fluid Lymphatic capillary 2 Fluid inside the lymphatic capillaries, called lymph, flows through lymphatic vessels throughout the body. Adenoid Tonsil 4 Lymphatic vessels return lymph to the blood via two large ducts that drain into veins near the shoulders. Lymph nodes Blood capillary Spleen Peyer’s patches (small intestine) Tissue cells Lymphatic vessel 3 Within lymph nodes, microbes and foreign particles present in the circulating lymph encounter macrophages, dendritic cells, and lymphocytes, which carry out various defensive actions. Appendix Lymphatic vessels Figure 43.5 Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Lymph node Masses of lymphocytes and macrophages Antimicrobial Proteins • Numerous proteins function in innate defense – By attacking microbes directly of by impeding their reproduction Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • About 30 proteins make up the complement system – Which can cause lysis of invading cells and help trigger inflammation • Interferons – Provide innate defense against viruses and help activate macrophages Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Inflammatory Response • In local inflammation, histamine and other chemicals released from injured cells – Promote changes in blood vessels that allow more fluid, more phagocytes, and antimicrobial proteins to enter the tissues Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • Major events in the local inflammatory response Pathogen Blood clot Pin Macrophage Histamine & Chemokines Chemical signals Phagocytic cells Capillary Blood clotting elements Phagocytosis Red blood cell 1 Chemical signals released by activated macrophages and mast cells at the injury site cause nearby capillaries to widen and become more permeable. 2 Fluid, antimicrobial proteins, and clotting elements move from the blood to the site. Clotting begins. Figure 43.6 Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings 3 Chemokines released by various kinds of cells attract more phagocytic cells from the blood to the injury site. 4 Neutrophils and macrophages phagocytose pathogens and cell debris at the site, and the tissue heals. Natural Killer Cells • Natural killer (NK) cells – Patrol the body and attack virus-infected body cells and cancer cells – Trigger apoptosis in the cells they attack animation Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Invertebrate Immune Mechanisms • Many invertebrates defend themselves from infection – By many of the same mechanisms in the vertebrate innate response – Amoeboid cells called coelomocytes phagocytose foreign matter and – Sea star coelomocytes release IL-1 to stimulate coelomocyte proliferation. Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • Concept 43.2: In acquired immunity, lymphocytes provide specific defenses against infection • Acquired immunity – Is the body’s second major kind of defense – Involves the activity of lymphocytes Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • An antigen is any foreign molecule – That is specifically recognized by lymphocytes and elicits a response from them • A lymphocyte actually recognizes and binds – To just a small, accessible portion of the antigen called an epitope Antigenbinding sites Antibody A Antigen Antibody B Antibody C Figure 43.7 Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Epitopes (antigenic determinants) Antigen Recognition by Lymphocytes • The vertebrate body is populated by two main types of lymphocytes – B lymphocytes (B cells) and T lymphocytes (T cells) – Which circulate through the blood • The plasma membranes of both B cells and T cells – Have about 100,000 antigen receptor that all recognize the same epitope Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings B Cell Receptors for Antigens • B cell receptors – Bind to specific, intact antigens – Are often called membrane antibodies or membrane immunoglobulins Antigenbinding site Antigenbinding site Disulfide bridge Variable regions Light chain Constant regions C C Transmembrane region Plasma membrane Heavy chains B cell Figure 43.8a Cytoplasm of B cell (a) A B cell receptor consists of two identical heavy chains and two identical light chains linked by several disulfide bridges. Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings T Cell Receptors for Antigens and the Role of the MHC • Each T cell receptor – Consists of two different polypeptide chains AntigenBinding site Variable regions Constant regions V V C C Transmembrane region Plasma membrane a chain b chain Disulfide bridge Cytoplasm of T cell Figure 43.8b (b) A T cell receptor consists of one a chain and one b chain linked by a disulfide bridge. Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings T cell • Class I MHC molecules, found on almost all nucleated cells of the body – Display peptide antigens to cytotoxic T cells Infected cell Antigen fragment 1 1 A fragment of foreign protein (antigen) inside the cell associates with an MHC molecule and is transported to the cell surface. Class I MHC molecule 2 T cell receptor Figure 43.9a (a) Cytotoxic T cell Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings 2 The combination of MHC molecule and antigen is recognized by a T cell, alerting it to the infection. • Class II MHC molecules, located mainly on dendritic cells, macrophages, and B cells – Display antigens to helper T cells Microbe 1 A fragment of foreign protein (antigen) inside the cell associates with an MHC molecule and is transported to the cell surface. Antigenpresenting cell Antigen fragment 1 Class II MHC molecule 2 2 The combination of MHC molecule and antigen is recognized by a T cell, alerting it to the infection. Figure 43.9b Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings (b) T cell receptor Helper T cell • Newly formed lymphocytes are all alike – But they later develop into B cells or T cells, depending on where they continue their maturation Bone marrow Lymphoid stem cell Thymus T cell B cell Blood, lymph, and lymphoid tissues (lymph nodes, spleen, and others) Figure 43.10 Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Generation of Lymphocyte Diversity by Gene Rearrangement • Early in development, random, permanent gene rearrangement – Forms functional genes encoding the B or T cell antigen receptor chains Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Immunoglobulin gene rearrangement V4–V39 DNA of undifferentiated B cell V2 V1 V40 V3 J1 J2 J3 J4 J5 Intron C 1 Deletion of DNA between a V segment and J segment and joining of the segments DNA of differentiated B cell V1 V3 J5 Intron V2 C 2 Transcription of resulting permanently rearranged, functional gene pre-mRNA V3 J5 Intron 3 mRNA Cap V 3 J5 C RNA processing (removal of intron; addition of cap and poly (A) tail) C Poly (A) 4 Translation Light-chain polypeptide Figure 43.11 V C Variable Constant region region Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings B cell receptor B cell Testing and Removal of Self-Reactive Lymphocytes • As B and T cells are maturing in the bone and thymus – Their antigen receptors are tested for possible self-reactivity • Lymphocytes bearing receptors for antigens already present in the body – Are destroyed by apoptosis or rendered nonfunctional Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Clonal Selection of Lymphocytes • In a primary immune response – Binding of antigen to a mature lymphocyte induces the lymphocyte’s proliferation and differentiation, a process called clonal selection Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Clonal Selection Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • Concept 43.3: Humoral and cell-mediated immunity defend against different types of threats • Acquired immunity includes two branches – The humoral immune response involves the activation and clonal selection of B cells, resulting in the production of secreted antibodies – The cell-mediated immune response involves the activation and clonal selection of cytotoxic T cells Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • The roles of the major participants in the acquired immune response Cell-mediated immune response Humoral immune response First exposure to antigen Intact antigens Antigens engulfed and displayed by dendritic cells Antigens displayed by infected cells Activate Activate Activate B cell Memory B cells Secrete antibodies that defend against pathogens and toxins in extracellular fluid Copyright © 2005 Pearson Education, Figure 43.14 Inc. publishing as Benjamin Cummings Cytotoxic T cell Gives rise to Gives rise to Gives rise to Plasma cells Helper T cell Secreted cytokines activate Active and memory helper T cells Memory cytotoxic T cells Active cytotoxic T cells Defend against infected cells, cancer cells, and transplanted tissues Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • The role of helper T cells in acquired immunity 1 After a dendritic cell engulfs and degrades a bacterium, it displays bacterial antigen fragments (peptides) complexed with a class II MHC molecule on the cell surface. A specific helper T cell binds to the displayed complex via its TCR with the aid of CD4. This interaction promotes secretion of cytokines by the dendritic cell. Cytotoxic T cell Dendritic cell Bacterium Peptide antigen Class II MHC molecule Helper T cell Cell-mediated immunity (attack on infected cells) TCR 2 IL2 1 CD4 Dendritic cell 3 Cytokines IL1 2 Proliferation of the T cell, stimulated by cytokines from both the dendritic cell and the T cell itself, gives rise to a clone of activated helper T cells (not shown), all with receptors for the same MHC–antigen complex. Figure 43.15 Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings B cell 3 The cells in this clone secrete other cytokines that help activate B cells and cytotoxic T cells. Humoral immunity (secretion of antibodies by plasma cells) animation animation • The activated cytotoxic T cell – Secretes proteins that destroy the infected target cell 2 The activated T cell releases perforin 1 A specific cytotoxic T cell binds to a molecules, which form pores in the class I MHC–antigen complex on a target cell membrane, and proteolytic target cell via its TCR with the aid of enzymes (granzymes), which enter the CD8. This interaction, along with target cell by endocytosis. cytokines from helper T cells, leads to the activation of the cytotoxic cell. Cytotoxic T cell 3 The granzymes initiate apoptosis within the target cells, leading to fragmentation of the nucleus, release of small apoptotic bodies, and eventual cell death. The released cytotoxic T cell can attack other target cells. Released cytotoxic T cell Perforin animation Cancer cell Granzymes 1 TCR Class I MHC molecule Target cell 3 CD8 2 Apoptotic target cell Pore Peptide antigen Figure 43.16 Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Cytotoxic T cell Overview animation What kind of MHC molecule? What kind of CD molecule? Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings B Cells: A Response to Extracellular Pathogens • Activation of B cells – Is aided by cytokines and antigen binding to helper T cells – Most antigens are Tdependent, meaning T cell help is required for maximal antibody production Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings H 1 After a macrophage engulfs and degrades 2 a bacterium, it displays a peptide antigen complexed with a class II MHC molecule. A helper T cell that recognizes the displayed complex is activated with the aid of cytokines secreted from the macrophage, forming a clone of activated helper T cells (not shown). A B cell that has taken up and degraded the same bacterium displays class II MHC–peptide antigen complexes. An activated helper T cell bearing receptors specific for the displayed antigen binds to the B cell. This interaction, with the aid of cytokines from the T cell, activates the B cell. 3 The activated B cell proliferates and differentiates into memory B cells and antibody-secreting plasma cells. The secreted antibodies are specific for the same bacterial antigen that initiated the response. Bacterium Macrophage Peptide antigen Class II MHC molecule B cell 2 3 1 TCR Clone of plasma cells Endoplasmic reticulum of plasma cell CD4 Cytokines Helper T cell animation Secreted antibody molecules Activated helper T cell Figure 43.17 Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Clone of memory B cells • The five classes of immunoglobulins IgM (pentamer) First Ig class produced after initial exposure to antigen; then its concentration in the blood declines J chain Promotes neutralization and agglutination of antigens; very effective in complement activation (see Figure 43.19) Most abundant Ig class in blood; also present in tissue fluids Only Ig class that crosses placenta, thus conferring passive immunity on fetus IgG (monomer) Promotes opsonization, neutralization, and agglutination of antigens; less effective in complement activation than IgM (see Figure 43.19) Present in secretions such as tears, saliva, mucus, and breast milk IgA (dimer) J chain Secretory component Provides localized defense of mucous membranes by agglutination and neutralization of antigens (see Figure 43.19) Presence in breast milk confers passive immunity on nursing infant IgE (monomer) IgD (monomer) Triggers release from mast cells and basophils of histamine and other chemicals that cause allergic reactions (see Figure 43.20) Present primarily on surface of naive B cells that have not been exposed to antigens Acts as antigen receptor in antigen-stimulated proliferation and differentiation of B cells (clonal Transmembrane selection) regionInc. publishing as Benjamin Cummings Copyright © 2005 Pearson Education, Figure 43.18 • Antibody-mediated mechanisms of antigen disposal Binding of antibodies to antigens inactivates antigens by Viral neutralization (blocks binding to host) and opsonization (increases phagocytosis) Agglutination of antigen-bearing particles, such as microbes Precipitation of soluble antigens Complement proteins Bacteria Virus Activation of complement system and pore formation MAC Pore Soluble antigens Bacterium Foreign cell Antimicrobial proteins Enhances Phagocytosis NO CAP CopyrightFigure © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Macrophage 43.19 Leads to Cell lysis Active immunity – Develops naturally in response to an infection – Can also develop following immunization, also called vaccination – Long term effects because memory cells are produced Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • In immunization – A nonpathogenic form of a microbe or part of a microbe elicits an immune response to an immunological memory for that microbe Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Passive immunity • provides immediate, short-term protection – Is conferred naturally when IgG crosses the placenta from mother to fetus or when IgA passes from mother to infant in breast milk – Can be conferred artificially by injecting antibodies into a nonimmune person Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Monoclonal Antibodies • Passive immunity can be obtained artificially by making monoclonal antibodies made to attack a specific antigen. animation Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings B lymphocyte • Concept 43.4: The immune system’s ability to distinguish self from nonself limits tissue transplantation • The immune system – Can wage war against cells from other individuals • Transplanted tissues – Are usually destroyed by the recipient’s immune system Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Blood Groups and Transfusions • Certain antigens on red blood cells – Determine whether a person has type A, B, AB, or O blood Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • Antibodies to nonself blood types – Already exist in the body • Transfusion with incompatible blood – Leads to destruction of the transfused cells Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • Recipient-donor combinations – Can be fatal or safe Table 43.1 Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • Another red blood cell antigen, the Rh factor – Creates difficulties when an Rh-negative mother carries successive Rh-positive fetuses Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Tissue and Organ Transplants • MHC molecules – Are responsible for stimulating the rejection of tissue grafts and organ transplants Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • The chances of successful transplantation are increased – If the donor and recipient MHC tissue types are well matched – If the recipient is given immunosuppressive drugs Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • Lymphocytes in bone marrow transplants – May cause a graft versus host reaction in recipients Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • Concept 43.5: Exaggerated, self-directed, or diminished immune responses can cause disease • If the delicate balance of the immune system is disrupted – The effects on the individual can range from minor to often fatal consequences Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Allergies • Allergies are exaggerated (hypersensitive) responses – To certain antigens called allergens Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • In localized allergies such as hay fever – IgE antibodies produced after first exposure to an allergen attach to receptors on mast cells – The next time the allergen enters the body – It binds to mast cell–associated IgE molecules • The mast cells then release histamine and other mediators – That cause vascular changes and typical symptoms Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • 2nd exposure triggers the mast cell to degranulate - that is, to release histamines and other inflammatory agents from vesicles called granules. 1st event 2nd Event Fig. 43.18 Copyright © 2005©Pearson Education,Education, Inc. publishing as Benjamin Cummings Copyright 2002 Pearson Inc., publishing as Benjamin Cummings • An acute allergic response sometimes leads to anaphylactic shock – A whole-body, life-threatening reaction that can occur within seconds of exposure to an allergen Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Autoimmune Diseases • In individuals with autoimmune diseases – The immune system loses tolerance for self and turns against certain molecules of the body Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • Rheumatoid arthritis – Is an autoimmune disease that leads to damage and painful inflammation of the cartilage and bone of joints Figure 43.21 Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • Other examples of autoimmune diseases include – Systemic lupus erythematosus – Multiple sclerosis – Insulin-dependent diabetes Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Immunodeficiency Diseases • An inborn or primary immunodeficiency – Results from hereditary or congenital defects that prevent proper functioning of innate, humoral, and/or cell-mediated defenses Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • An acquired or secondary immunodeficiency – Results from exposure to various chemical and biological agents Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Inborn (Primary) Immunodeficiencies • In severe combined immunodeficiency (SCID) – Both the humoral and cell-mediated branches of acquired immunity fail to function Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Acquired (Secondary) Immunodeficiencies • Acquired immunodeficiencies – Range from temporary states to chronic diseases Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Stress and the Immune System • Growing evidence shows – That physical and emotional stress can harm immunity Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • Acquired Immunodeficiency Syndrome (AIDS) • People with AIDS – Are highly susceptible to opportunistic infections and cancers that take advantage of an immune system in collapse Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • Because AIDS arises from the loss of helper T cells – Both humoral and cell-mediated immune responses are impaired Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • The loss of helper T cells – Results from infection by the human immunodeficiency virus (HIV) Figure 43.22 Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings 1µm 1 After a macrophage engulfs and degrades 2 a bacterium, it displays a peptide antigen complexed with a class II MHC molecule. A helper T cell that recognizes the displayed complex is activated with the aid of cytokines secreted from the macrophage, forming a clone of activated helper T cells (not shown). A B cell that has taken up and degraded the same bacterium displays class II MHC–peptide antigen complexes. An activated helper T cell bearing receptors specific for the displayed antigen binds to the B cell. This interaction, with the aid of cytokines from the T cell, activates the B cell. 3 The activated B cell proliferates and differentiates into memory B cells and antibody-secreting plasma cells. The secreted antibodies are specific for the same bacterial antigen that initiated the response. Bacterium Macrophage Peptide antigen Class II MHC molecule B cell 2 3 1 TCR Clone of plasma cells Endoplasmic reticulum of plasma cell CD4 Cytokines Helper T cell Secreted antibody molecules Activated helper T cell Figure 43.17 Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Clone of memory B cells • The spread of HIV – Has become a worldwide problem • The best approach for slowing the spread of HIV – Is educating people about the practices that transmit the virus Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings 33.2 million people have AIDS worldwide Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings • There are two major strains of the virus, HIV-1 and HIV-2. – HIV-1 is the more widely distributed and more virulent. • Both strains infect cells that bear CD4 molecules, especially helper T cells and class II MCH-bearing antigen-presenting cells, but also macrophages, some lymphocytes and some brain cells. – CD4 functions as the major receptor for the virus. Copyright © 2005©Pearson Education,Education, Inc. publishing as Benjamin Cummings Copyright 2002 Pearson Inc., publishing as Benjamin Cummings • The entry of the virus requires not only CD4 on the surface of the susceptible cells but also a second protein molecule, a coreceptor. – Two of the coreceptors (fusin and CCR5) that have been identified normally function as receptors for chemokines. – Some people who are innately resistant to HIV1 owe their resistance to defective chemokine receptors which prevents HIV from binding and infecting cells. Copyright © 2005©Pearson Education,Education, Inc. publishing as Benjamin Cummings Copyright 2002 Pearson Inc., publishing as Benjamin Cummings