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Immunity. Chapter 23. Smallpox Vaccine. Before vaccines, smallpox had up to 50% death rates Now smallpox is practically eradicated. Immunity. Body’s ability to resist and combat diseases Depends on mechanisms that recognize proteins as self or nonself Antigen
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Immunity Chapter 23
Smallpox Vaccine • Before vaccines, smallpox had up to 50% death rates • Now smallpox is practically eradicated
Immunity • Body’s ability to resist and combat diseases • Depends on mechanisms that recognize proteins as self or nonself • Antigen • Any molecule the body recognizes as nonself and provokes an immune response
Evolution of Defenses • Innate immunity • Preset responses to nonself cues • Complement, phagocytes • Adaptive immunity • Prepares defenses to specific pathogens encountered during an individual’s lifetime • Cytokines, lymphocytes
Three Lines of Defense • Physical barriers • exclude pathogens • Innate immunity • begins as soon as antigen is detected • Adaptive immunity • forms cells that fight infection and prevent later infection
White Blood Cells • Form in bone marrow • Participate in adaptive and innate responses • Release cytokines and other cell-to-cell signaling molecules
White Blood Cells basophil mast cell neutrophil eosinophil
White Blood Cells NK cell B lymphocyte T lymphocyte
White Blood Cells dendritic cell macrophage
Surface Barriers • Physical barriers • Intact skin • Mechanical barriers • Mucus, cilia, flushing • Chemical barriers • Protective secretions, low pH, lysozyme
Innate Immune Response • Phagocytosis • Complement • Fever • Acute inflammation
Complement • Many types of circulating proteins • Activated by binding to antigen • Triggers reactions that activate more complement • Attract phagocytic cells
Membrane Attack Complexes lipid bilayer of pathogen antibody activated complement bacterial pathogen Cascade reactions Formation of attack complexes Lysis of target Activation
one membrane attack complex (cutaway view) lipid bilayer of one kind of pathogen hole in the plasma membrane of an unlucky baterium Fig. 23-6, p.388
Acute Inflammation • Nonspecific response to foreign invasion, tissue damage • Destroys invaders, removes debris • Symptoms are redness, swelling, warmth, and pain
Inflammation • Mast cells release histamine • Capillaries dilate and leak • Complement proteins attack bacteria • White cells attack invaders and clean up
d Complement proteins attack bacteria. Clotting factors wall off inflamed area. b Mast cells in tissue release histamines, which then trigger arteriole vasodilation (hence redness and warmth) as well as increased capillary permeability. c Fluid and plasma proteins leak out of capillaries; localized edema (tissue swelling) and pain result. e Neutrophils, macrophages, engulf invaders and debris.Some macrophage secretions kill targets, attract more lymphocytes, and call for fever. a Bacteria invade a tissue and directly kill cells or release metabolic products that damage tissue. Fig. 23-7, p.388
Fever • Temperature up to 39°C (102°F) • Enhances immunity, increases rates of enzyme and phagocyte activity • Accelerates tissue repair
Features of Adaptive Immunity • Self/nonself recognition • Specificity • Diversity • Memory
Antigens • “Nonself” markers on foreign agents and altered body cells such as tumors • Trigger division of B and T cells
Memory and Effector Cells • When a B or T cell is stimulated to divide, it produces 2 cell types • Memory cells: set aside for future use • Effector cells: engage and destroy the current threat
Key Components of Immune Response • MHC markers • Antigen-presenting cells • T cells • B cells • Natural killer (NK) cells
Formation of Antigen–MHC Complex antigen fragments MHC molecule antigen–MHC complex
fragments of engulfed antigen MHC marker that the cell already made antigen-MHC complex displayed at surface of plasma membrane Fig. 23-9, p.390
Key Interactions Antibody-Mediated Immune Response Cell-Mediated Immune Response antigen-presenting cells naive B cells + antigen + complement naive helper T cells activated B cells naive cytotoxic T cells effector helper T cells + memory helper T cells effector B cells + memory B cells effector cytotoxic T cells + memory cytotoxic cells Fig. 23-10, p.390
Antigen Interception • Antigen-presenting T cells are trapped in lymph nodes • Macrophages, dendritic cells, and B cells bind, process and present antigen
TONSILS RIGHT LYMPHATIC DUCT THYMUS GLAND THORACIC DUCT SPLEEN SOME OF THE LYMPH VESSELS SOME OF THE LYMPH NODES BONE MARROW Fig. 23-11a, p.391
arrays of lymphocytes valve (prevents backflow) Fig. 23-11b, p.391
Antigen Receptors • Antibodies • Synthesized by B cells • Bind to one specific antigen • Mark pathogen for destruction by phagocytes and complement proteins
Antibody Structure • Consists of four polypeptide chains • Parts of each chain are variable; provide antigen specificity antigen binding site variable region constant region
binding site for antigen binding site for antigen variable region (dark green) of heavy chain variable region of light chain constant region (bright green) of heavy chain, that includes a hinged region Fig. 23-12a, p.392
antigen on bacterial cell (not to scale) binding site on one kind of antibody molecule for a specific antigen Fig. 23-12b, p.392
antigen on virus particle binding site on another kind of antibody molecule For a different antigen Fig. 23-12c, p.392
Immunoglobins (Igs) • Five classes of antibodies • IgG • IgA • IgE • IgM • IgD
Antigen Receptor Diversity a As a B cell matures, different segments of antibody-coding genes recombine at random into a final gene sequence. b The final sequence is transcribed into mRNA. c Processing yields a mature mRNA transcript (e.g., introns excised, exons spliced). d mRNA is translated into one of the polypeptide chains of an antibody molecule. Stepped Art Fig. 23-13, p.393
Antibody-Mediated Immune Response • B cell responds to one particular extracellular pathogen or toxin • Activated B cell forms clones that differentiate into effector and memory cells • Effector B cells secrete antibodies that tag antigens for destruction
B Cell Division antigen Antigen binds only to antibody specific to it on a naive B cell. clonal population of effector B cells Effector B cells secrete antibodies. Fig. 23-15a, p.395
B Cell Differentiation First exposure to antigen provokes a primary immune response. naive B cell effector cells memory cells Another exposure to the same antigen provokes secondary response. effector cells memory cells Fig. 23-15b, p.395
Secondary Immune Response Fig. 23-15c, p.395
Cell-Mediated Immune Response • Cytotoxic T cells target altered body cells that evade antibody-mediated immune response • Antigen-presenting dendritic cells activate helper T cells
Cell-Mediated Immune Response • Helper T cells secrete cytokines • Induce formation of cytotoxic T cells • Proliferate NK cells • Enhance macrophage activity • Destroy infected or altered cells
Cell-Mediated Immune Response cytotoxic T-cell tumor cell
Immunization • Process that induces immunity • Active immunization: • Vaccination with antigen • Long-lasting immunity • Passive immunization: • Purified antibody is injected • Protection is short lived