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Figure 21.1 Overview of innate and adaptive defenses.
Surface barriers • Skin • Mucous membranes Innate defenses Internal defenses • Phagocytes • Natural killer cells • Inflammation • Antimicrobial proteins • Fever Humoral immunity • B cells Adaptive defenses Cellular immunity • T cells © 2013 Pearson Education, Inc.
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Innate defenses Internal defenses
Figure Phagocytosis. Phagocyte adheres to pathogens or debris. 1 Innate defenses Internal defenses Phagocyte forms pseudopods that eventually engulf the particles, forming a phagosome. 2 Phagosome (phagocytic vesicle) Lysosome Lysosome fuses with the phagocytic vesicle, forming a phagolysosome. 3 Acid hydrolase enzymes Lysosomal enzymes digest the particles, leaving a residual body. 4 A macrophage (purple) uses its cytoplasmic extensions to pull rod-shaped bacteria (green) toward it. Scanning electron micrograph (4800x). Exocytosis of the vesicle removes indigestible and residual material. 5 Events of phagocytosis. © 2013 Pearson Education, Inc.
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Figure 21.3 Inflammation: flowchart of events.
Innate defenses Internal defenses Initial stimulus Physiological response Signs of inflammation Tissue injury Result Release of inflammatory chemicals (histamine, complement, kinins, prostaglandins, etc.) Release of leukocytosis- inducing factor Leukocytosis (increased numbers of white blood cells in bloodstream) Arterioles dilate Increased capillary permeability Attract neutrophils, monocytes, and lymphocytes to area (chemotaxis) Leukocytes migrate to injured area Local hyperemia (increased blood flow to area) Capillaries leak fluid (exudate formation) Margination (leukocytes cling to capillary walls) Diapedesis (leukocytes pass through capillary walls) Leaked protein-rich fluid in tissue spaces Leaked clotting proteins form interstitial clots that wall off area to prevent injury to surrounding tissue Phagocytosis of pathogens and dead tissue cells (by neutrophils, short-term; by macrophages, long-term) Heat Redness Pain Swelling Locally increased temperature increases metabolic rate of cells Possible temporary impairment of function Temporary fibrin patch forms scaffolding for repair Pus may form Area cleared of debris Healing © 2013 Pearson Education, Inc.
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Figure 21.4 Phagocyte mobilization.
Innate defenses Internal defenses Inflammatory chemicals diffusing from the inflamed site act as chemotactic agents. Chemotaxis. Neutrophils follow chemical trail. 4 Capillary wall Basement membrane Endothelium Leukocytosis. Neutrophils enter blood from bone marrow. 1 Margination. Neutrophils cling to capillary wall. 2 Diapedesis. Neutrophils flatten and squeeze out of capillaries. 3 © 2013 Pearson Education, Inc.
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Table 21.1 Inflammatory Chemicals
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Table 21.2 Summary of Innate Body Defenses (1 of 2)
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Table 21.2 Summary of Innate Body Defenses (2 of 2)
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Figure 21.6 Complement activation.
Classical pathway Lectin pathway Alternative pathway Activated by antibodies coating target cell Activated by lectins binding to specific sugars on microorganism’s surface Activated spontaneously. Lack of inhibitors on microorganism’s surface allows process to proceed Together with other complement proteins and factors C3 C3a C3b C3b Opsonization: Enhances inflammation: C5b C5a Coats pathogen surfaces, which enhances phagocytosis Stimulates histamine release, increases blood vessel permeability, attracts phagocytes by chemotaxis, etc. C6 MAC C7 C8 C9 MACs form from activated complement components (C5b and C6–C9) that insert into the target cell membrane, creating pores that can lyse the target cell. Pore Complement proteins (C5b–C9) Membrane of target cell © 2013 Pearson Education, Inc.
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Figure 21.8 Lymphocyte development, maturation, and activation.
Humoral immunity Primary lymphoid organs (red bone marrow and thymus) Adaptive defenses Cellular immunity Secondary lymphoid organs (lymph nodes, spleen, etc.) Red bone marrow Red bone marrow Origin • Both B and T lymphocyte precursors originate in red bone marrow. 1 Lymphocyte precursors Maturation • Lymphocyte precursors destined to become T cells migrate (in blood) to the thymus and mature there. • B cells mature in the bone marrow. • During maturation lymphocytes develop immunocompetence and self-tolerance. 2 Thymus Red bone marrow Seeding secondary lymphoid organs and circulation • Immunocompetent but still naive lymphocytes leave the thymus and bone marrow. • They “seed” the secondary lymphoid organs and circulate through blood and lymph. 3 Antigen Antigen encounter and activation • When a lymphocyte’s antigen receptors bind its antigen, that lymphocyte can be activated. 4 Lymph node Proliferation and differentiation • Activated lymphocytes proliferate (multiply) and then differentiate into effector cells and memory cells. • Memory cells and effector T cells circulate continuously in the blood and lymph and throughout the secondary lymphoid organs. 5 © 2013 Pearson Education, Inc.
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Figure 21.9 T cell education in the thymus.
Adaptive defenses Cellular immunity 1. Positive Selection T cells must recognize self major histocompatibility proteins (self-MHC) Antigen- presenting thymic cell Developing T cell Failure to recognize self- MHC results in apoptosis (death by cell suicide). Self-MHC T cell receptor Self-antigen Recognizing self-MHC results in survival. Survivors proceed to negative selection. 2. Negative Selection T cells must not recognize self-antigens Recognizing self-antigen results in apoptosis. This eliminates self-reactive T cells that could cause autoimmune diseases. Failure to recognize (bind tightly to) self-antigen results in survival and continued maturation. © 2013 Pearson Education, Inc.
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Figure 21.11 Clonal selection of a B cell.
Adaptive defenses Humoral immunity Primary response (initial encounter with antigen) Antigen Antigen binding to a receptor on a specific B lymphocyte (B lymphocytes with noncomplementary receptors remain inactive) Proliferation to form a clone Activated B cells Plasma cells (effector B cells) Memory B cell— primed to respond to same antigen Secreted antibody molecules Secondary response (can be years later) Subsequent challenge by same antigen results in more rapid response Clone of cells identical to ancestral cells Plasma cells Secreted antibody molecules Memory B cells © 2013 Pearson Education, Inc.
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Table 21.3 Overview of B and T Lymphocytes
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Ex. Immunization or vaccinated for polio
Humoral immunity Active Passive Naturally acquired Infection; contact with pathogen Artificially Vaccine; dead or attenuated pathogens Antibodies passed from mother to fetus via placenta; or to infant in her milk Injection of exogenous antibodies (gamma globulin) Ex. Catching a cold Ex. Immunization or vaccinated for polio Ex. Antibodies cross placenta to fetus Ex. Anti-tetanus injection “Induced” © 2013 Pearson Education, Inc.
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Figure 21.15 Mechanisms of antibody action.
Adaptive defenses Humoral immunity Antigen-antibody complex Antigen Antibody Inactivates by Fixes and activates Neutralization (masks dangerous parts of bacterial exotoxins; viruses) Agglutination (cell-bound antigens) Precipitation (soluble antigens) Complement Enhances Enhances Leads to Phagocytosis Inflammation Cell lysis Chemotaxis Histamine release © 2013 Pearson Education, Inc.
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Table 21.4 Immunoglobulin Classes (1 of 2)
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Table 21.4 Immunoglobulin Classes (2 of 2)
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Figure 21.16 Major types of T cells.
Adaptive defenses Cellular immunity Immature lymphocyte Red bone marrow T cell receptor T cell receptor Maturation Class II MHC protein displaying antigen CD8 cell Class I MHC protein displaying antigen CD4 cell Thymus Activation Activation APC (dendritic cell) Memory cells APC (dendritic cell) CD4 CD8 CD4 cells become either helper T cells or regulatory T cells Lymphoid tissues and organs CD8 cells become cytotoxic T cells Effector cells Blood plasma © 2013 Pearson Education, Inc.
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Table 21.5 Role of MHC Proteins in Cellular Immunity
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Figure 21.17 Clonal selection of T cells involves simultaneous recognition of self and nonself.
Adaptive defenses Cellular immunity Bacterial antigen Antigen presentation Dendritic cell engulfs an exogenous antigen, processes it, and displays its fragments on class II MHC protein. 1 Class lI MHC protein displaying processed bacterial antigen Dendritic cell Co-stimulatory molecule CD4 protein 2 Double recognition T cell receptor (TCR) CD4 T cell recognizes antigen- MHC complex. Both TCR and CD4 proteins bind to antigen-MHC complex. 2a Co-stimulatory molecules CD4 T cell Co-stimulatory molecules bind together. 2b Clone formation Clone formation Activated CD4 T cells proliferate (clone), and become memory and effector cells. 3 Memory CD4 T cell Helper T cells © 2013 Pearson Education, Inc.
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B cell (being activated)
Figure The central role of helper T cells in mobilizing both humoral and cellular immunity. Humoral immunity Adaptive defenses Cellular immunity Helper T cells help in humoral immunity Helper T cells help in cellular immunity Helper T cell CD4 protein Helper T cell TH cell binds dendritic cell. Class II MHC protein 1 TH cell binds with the self-nonself complexes of a B cell that has encountered its antigen and is displaying it on MHC II on its surface. 1 T cell receptor (TCR) APC (dendritic cell) Helper T cell CD4 protein TH cell stimulates dendritic cell to express co-stimulatory molecules. 2 IL-2 MHC II protein of B cell displaying processed antigen TH cell releases interleukins as co- stimulatory signals to complete B cell activation. 2 Dendritic cell can now activate CD8 cell with the help of interleukin 2 secreted by TH cell. IL-4 and other cytokines 3 Class I MHC protein CD8 protein CD8 T cell (becomes TC cell after activation) B cell (being activated) © 2013 Pearson Education, Inc.
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Figure 21.19 Cytotoxic T cells attack infected and cancerous cells.
Adaptive defenses Cellular immunity Cytotoxic T cell (TC) TC identifies foreign antigens on MHC I proteins and binds tightly to target cell. 1 TC releases perforin and granzyme molecules from its granules by exocytosis. 2 Perforin molecules insert into the target cell membrane, polymerize, and form transmembrane pores (cylindrical holes) similar to those produced by complement activation. 3 Granule Perforin TC cell membrane Cytotoxic T cell Target cell membrane Target cell Perforin pore Cancer cell Granzymes Granzymes enter the target cell via the pores. Once inside, granzymes activate enzymes that trigger apoptosis. 4 The TC detaches and searches for another prey. 5 A mechanism of target cell killing by TC cells. Scanning electron micrograph of a TC cell killing a cancer cell (2100x). © 2013 Pearson Education, Inc.
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Table 21.6 Selected Cytokines
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Figure 21.20 Simplified summary of the primary immune response.
Cellular immunity Humoral immunity Antigen (Ag) intruder Inhibits Triggers Inhibits Adaptive defenses Innate defenses Surface barriers Internal defenses Free Ags may directly activate B cell Ag-infected body cell engulfed by dendritic cell Antigen- activated B cells Becomes Clone and give rise to Ag-presenting cell (APC) presents self-Ag complex Co-stimulate and release cytokines Present Ag to activated helper T cells Activates Activates Memory B cells Naive CD8 T cells Naive CD4 T cells Activated to clone and give rise to Activated to clone and give rise to Induce co-stimulation Plasma cells (effector B cells) Memory CD8 T cells Memory CD4 T cells Secrete Cytotoxic T cells Helper T cells Cytokines stimulate Nonspecific killers (macrophages and NK cells of innate immunity) Antibodies (Igs) Together the nonspecific killers and cytotoxic T cells mount a physical attack on the Ag Circulating lgs along with complement mount a chemical attack on the Ag © 2013 Pearson Education, Inc.
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Table 21.7 Cells and Molecules of the Adaptive Immune Response (1 of 2)
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Table 21.7 Cells and Molecules of the Adaptive Immune Response (2 of 2)
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Figure 21.21 Mechanism of an acute allergic (immediate hypersensitivity) response.
Adaptive defenses Humoral immunity Sensitization stage Antigen Antigen (allergen) invades body. 1 Plasma cells produce large amounts of class IgE antibodies against allergen. 2 Mast cell with fixed IgE antibodies IgE IgE antibodies attach to mast cells in body tissues (and to circulating basophils). 3 Granules containing histamine Subsequent (secondary) responses More of same antigen invades body. 4 Mast cell granules release contents after antigen binds with IgE antibodies Antigen combines with IgE attached to mast cells (and basophils), which triggers degranulation and release of histamine (and other chemicals). 5 Histamine Histamine causes blood vessels to dilate and become leaky, which promotes edema; stimulates secretion of large amounts of mucus; and causes smooth muscles to contract. (If respiratory system is site of antigen entry, asthma may ensue.) 6 Outpouring of fluid from capillaries Release of mucus Constriction of small respiratory passages (bronchioles) © 2013 Pearson Education, Inc.
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