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Copyright © 2010 Pearson Education, Inc. Figure 21.1 Innate defenses Surface barriers Skin Mucous membranes Internal defenses Phagocytes NK cells Inflammation.

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Presentation on theme: "Copyright © 2010 Pearson Education, Inc. Figure 21.1 Innate defenses Surface barriers Skin Mucous membranes Internal defenses Phagocytes NK cells Inflammation."— Presentation transcript:

1 Copyright © 2010 Pearson Education, Inc. Figure 21.1 Innate defenses Surface barriers Skin Mucous membranes Internal defenses Phagocytes NK cells Inflammation Antimicrobial proteins Fever Humoral immunity B cells Cellular immunity T cells Adaptive defenses

2 Copyright © 2010 Pearson Education, Inc. Inflammatory Response Macrophages and epithelial cells of boundary tissues bear Toll-like receptors (TLRs) TLRs recognize specific classes of infecting microbes Activated TLRs trigger the release of cytokines that promote inflammation

3 Copyright © 2010 Pearson Education, Inc. Phagocyte Mobilization Steps for phagocyte mobilization 1.Leukocytosis: release of neutrophils from bone marrow in response to leukocytosis-inducing factors from injured cells 2.Margination: neutrophils cling to the walls of capillaries in the inflamed area 3.Diapedesis of neutrophils 4.Chemotaxis: inflammatory chemicals (chemotactic agent) promote positive chemotaxis of neutrophils

4 Copyright © 2010 Pearson Education, Inc. Figure 21.3 Tissue injury Release of chemical mediators (histamine, complement, kinins, prostaglandins, etc.) Vasodilation of arterioles Increased capillary permeability Local hyperemia (increased blood flow to area) Locally increased temperature increases metabolic rate of cells Leaked protein-rich fluid in tissue spaces Leaked clotting proteins form interstitial clots that wall off area to prevent injury to surrounding tissue Temporary fibrin patch forms scaffolding for repair Healing Capillaries leak fluid (exudate formation) Attract neutrophils, monocytes, and lymphocytes to area (chemotaxis) Release of leukocytosis- inducing factor Leukocytosis (increased numbers of white blood cells in bloodstream) Leukocytes migrate to injured area Margination (leukocytes cling to capillary walls) Diapedesis (leukocytes pass through capillary walls) Phagocytosis of pathogens and dead tissue cells (by neutrophils, short-term; by macrophages, long-term) Area cleared of debris Pus may form Signs of inflammation Initial stimulus Physiological response Result Innate defensesInternal defenses Possible temporary limitation of joint movement HeatRedness PainSwelling

5 Copyright © 2010 Pearson Education, Inc. Phagocyte Mobilization Steps for phagocyte mobilization 1.Leukocytosis: release of neutrophils from bone marrow in response to leukocytosis-inducing factors from injured cells 2.Margination: neutrophils cling to the walls of capillaries in the inflamed area 3.Diapedesis of neutrophils 4.Chemotaxis: inflammatory chemicals (chemotactic agent) promote positive chemotaxis of neutrophils

6 Copyright © 2010 Pearson Education, Inc. Figure 21.4, step 1 Innate defenses Internal defenses Leukocytosis. Neutrophils enter blood from bone marrow. Capillary wall Basement membrane Endothelium Inflammatory chemicals diffusing from the inflamed site act as chemotactic agents. 1

7 Copyright © 2010 Pearson Education, Inc. Figure 21.4, step 2 Innate defenses Internal defenses Leukocytosis. Neutrophils enter blood from bone marrow. Margination. Neutrophils cling to capillary wall. Capillary wall Basement membrane Endothelium Inflammatory chemicals diffusing from the inflamed site act as chemotactic agents. 12

8 Copyright © 2010 Pearson Education, Inc. Figure 21.4, step 3 Innate defenses Internal defenses Leukocytosis. Neutrophils enter blood from bone marrow. Margination. Neutrophils cling to capillary wall. Diapedesis. Neutrophils flatten and squeeze out of capillaries. Capillary wall Basement membrane Endothelium Inflammatory chemicals diffusing from the inflamed site act as chemotactic agents. 123

9 Copyright © 2010 Pearson Education, Inc. Figure 21.4, step 4 Innate defenses Internal defenses Leukocytosis. Neutrophils enter blood from bone marrow. Margination. Neutrophils cling to capillary wall. Diapedesis. Neutrophils flatten and squeeze out of capillaries. Chemotaxis. Neutrophils follow chemical trail. Capillary wall Basement membrane Endothelium Inflammatory chemicals diffusing from the inflamed site act as chemotactic agents

10 Copyright © 2010 Pearson Education, Inc. Adaptive Defenses Adaptive immune response Is specific Is systemic Has memory Two separate overlapping arms 1.Humoral (antibody-mediated) immunity 2.Cellular (cell-mediated) immunity

11 Copyright © 2010 Pearson Education, Inc. Antigens Substances that can mobilize the adaptive defenses and provoke an immune response Most are large, complex molecules not normally found in the body (nonself)

12 Copyright © 2010 Pearson Education, Inc. Antigenic Determinants Parts of antigen that are immunogenic Antibodies and lymphocyte receptors bind to them

13 Copyright © 2010 Pearson Education, Inc. Figure 21.7 Antigenic determinants Antigen- binding sites Antibody A Antibody B Antibody C Antigen

14 Copyright © 2010 Pearson Education, Inc. Haptens (Incomplete Antigens) Small molecules (peptides, nucleotides, and hormones) Not immunogenic by themselves Are immunogenic when attached to body proteins Cause the immune system to mount a harmful attack Examples: poison ivy, animal dander, detergents, and cosmetics

15 Copyright © 2010 Pearson Education, Inc. Self-Antigens: MHC Proteins Proteins (self-antigens) on cell surface of s Example: MHC proteins Coded for by genes of major histocompatibility complex (MHC) and unique

16 Copyright © 2010 Pearson Education, Inc. MHC Proteins Classes Class I MHC proteins, on most all cells Class II MHC proteins, on certain cells in immune response

17 Copyright © 2010 Pearson Education, Inc. Cells of the Adaptive Immune System Two types of lymphocytes B lymphocytes (B cells)—humoral immunity T lymphocytes (T cells)—cell-mediated immunity Antigen-presenting cells (APCs) Do not respond to specific antigens Play essential auxiliary roles in immunity

18 Copyright © 2010 Pearson Education, Inc. Figure Red bone marrow: site of lymphocyte origin Secondary lymphoid organs: site of antigen encounter, and activation to become effector and memory B or T cells Primary lymphoid organs: site of development of immunocompetence as B or T cells Lymphocytes destined to become T cells migrate (in blood) to the thymus and develop immunocompetence there. B cells develop immunocompetence in red bone marrow. Immunocompetent but still naive lymphocytes leave the thymus and bone marrow. They “seed” the lymph nodes, spleen, and other lymphoid tissues where they encounter their antigen. Antigen-activated immunocompetent lymphocytes (effector cells and memory cells) circulate continuously in the bloodstream and lymph and throughout the lymphoid organs of the body. Red bone marrow Bone marrow Thymus Lymph nodes, spleen, and other lymphoid tissues Immature lymphocytes Adaptive defenses Humoral immunity Cellular immunity

19 Copyright © 2010 Pearson Education, Inc. T Cells T cells mature in the thymus under negative and positive selection pressures Positive selection Selects T cells capable of binding to self- MHC proteins (MHC restriction) Negative selection Prompts apoptosis of T cells that bind to self-antigens displayed by self-MHC Ensures self-tolerance

20 Copyright © 2010 Pearson Education, Inc. Figure 21.9 Adaptive defenses Positive selection: T cells must recognize self major histocompatibility proteins (self-MHC). Antigen- presenting thymic cell Failure to recognize self-MHC results in apoptosis (death by cell suicide). Recognizing self-MHC results in MHC restriction —survivors are restricted to recognizing antigen on self-MHC. Survivors proceed to negative selection. 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. MHC Self-antigen T cell receptor Developing T cell Cellular immunity Negative selection: T cells must not recognize self-antigens.

21 Copyright © 2010 Pearson Education, Inc. Antigen Receptor Diversity Lymphocytes make up to a billion different types of antigen receptors Coded for by ~25,000 genes Gene segments are shuffled by somatic recombination Genes determine which foreign substances the immune system will recognize and resist

22 Copyright © 2010 Pearson Education, Inc. Antigen-Presenting Cells (APCs) Engulf antigens Present fragments of antigens to T cells Major types Dendritic in connective tissues and epidermis Macrophages in connective tissues and lymphoid organs B cells

23 Copyright © 2010 Pearson Education, Inc. Macrophages and Dendritic Cells Present antigens and activate T cells Macrophages mostly remain fixed in the lymphoid organs Dendritic cells internalize pathogens and enter lymphatics to present the antigens to T cells in lymphoid organs Activated T cells release chemicals that Prod macrophages to become insatiable phagocytes and to secrete bactericidal chemicals

24 Copyright © 2010 Pearson Education, Inc. Figure (1 of 2) Primary response (initial encounter with antigen) Antigen binding to a receptor on a specific B lymphocyte (B lymphocytes with non-complementary receptors remain inactive) Proliferation to form a clone Activated B cells Plasma cells (effector B cells) Secreted antibody molecules Memory B cell— primed to respond to same antigen Adaptive defensesHumoral immunity Antigen

25 Copyright © 2010 Pearson Education, Inc. Clonal Selection 1.B cell is activated when antigens bind to its surface receptors and cross-link them 2.Receptor-mediated endocytosis of cross- linked antigen-receptor complexes occurs 3.Stimulated B cell grows to form a clone of identical cells bearing the same antigen- specific receptors (T cells are usually required to help B cells achieve full activation)

26 Copyright © 2010 Pearson Education, Inc. Fate of the Clones Secreted antibodies Circulate in blood or lymph Bind to free antigens Mark the antigens for destruction

27 Copyright © 2010 Pearson Education, Inc. Immunological Memory Primary immune response Occurs on the first exposure to a specific antigen Lag period: three to six days Peak levels of plasma antibody are reached in 10 days Antibody levels then decline

28 Copyright © 2010 Pearson Education, Inc. Figure Primary response (initial encounter with antigen) Antigen binding to a receptor on a specific B lymphocyte (B lymphocytes with non-complementary receptors remain inactive) Proliferation to form a clone Activated B cells Plasma cells (effector B cells) Secreted antibody molecules Memory B cell— primed to respond to same antigen Clone of cells identical to ancestral cells Subsequent challenge by same antigen results in more rapid response Secondary response (can be years later) Memory B cells Plasma cells Secreted antibody molecules Adaptive defensesHumoral immunity Antigen

29 Copyright © 2010 Pearson Education, Inc. Figure Time (days) Anti- bodies to A First exposure to antigen A Second exposure to antigen A; first exposure to antigen B Anti- bodies to B Primary immune response to antigen A occurs after a delay. Secondary immune response to antigen A is faster and larger; primary immune response to antigen B is similar to that for antigen A.

30 Copyright © 2010 Pearson Education, Inc. Figure Passive Active Humoral immunity Artificially acquired Injection of immune serum (gamma globulin) Naturally acquired Antibodies pass from mother to fetus via placenta; or to infant in her milk Artificially acquired Vaccine; dead or attenuated pathogens Naturally acquired Infection; contact with pathogen


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