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External and Internal Defenses
Immune System Chapter 35 External and Internal Defenses
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Phagocytic Cells = cells that engulf & digest antigens
Antigens =any foreign molecule recognized by a lymphocyte (B or T cell) a) most are proteins or polysaccharides b) may protrude from microbe membrane c) epitope = tiny part the lymphocyte binds
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MHC = major histocompatibility complex
Set of genes that code for MHC molecules All are cell surface proteins Class I MHC display foreign peptides synthesized within the cell (cancer/virus) found on most body cells Class II MHC display peptides broken off of microbes during phagocytosis found on phagocytic cells & B cells
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* Helper–T cells Type of T cell that binds to antigens displayed by phagocytic cells or B-cells (Class II MHC molecules) Helps promote acquired immune response Promote Humoral (B-cell) response by secreting cytokines Promote cell mediated-response (cytotoxic-T cells)
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External Defenses 1) Skin…waterproof layer dead cells
2) Linings of body tubes/cavities a) sticky mucus w/ lysozyme enzymes b) ciliated cells in resp. tract c) stomach acid & bile salts d) urine & vaginal low pH 3) Neutral/beneficial bacteria population
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Internal Defenses I. innate immunity =
present at birth, always present II. aquired/adaptive immunity = activated by microbes/antigens a) Require self-recognition (membrane proteins) b) only present in Vertebrates
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I. Innate Immunity A) Antimicrobial proteins B) inflammatory response
C) Systemic response D) Phagocytic Cells E) Natural Killer Cells
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A) Antimicrobial Proteins
1) interferon ά and β secreted by virus-infected cells help neighboring cells inhibit viral reproduction 2) complement system = 30 serum proteins a. microbe presence activates complement proteins b. cascade of chem rxns lead to c. microbe lysis d. plays a role in inflammation (complement syst also activated by acquired response)
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B) Inflammation Triggered by chem. signals: histamine & cytokine
Complement system, allergen, antigen or injury cause mast cells to release histamine Histamine dilates capillaries, lets out more clotting elements, anti-microbial proteins Chemokines released by capillary attract phagocytes (macrophages & neutrophiles) Macrophages secrete cytokines that promote blood flow Clotting blocks spread of microbes
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C) Systemic Response Widespread response Increased WBC production
Fever – facilitates phagocytosis Septic shock – bacterial infection causes high fever low bp may cause death
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D) Phagocytic cells (4 types)
1) neutrophils – most abundant (1st responders) 2) macrophages – largest 3) eosinophils – poison multi-cellular parasites 4) dentritic cells – activate acquired immunity a) digest pathogen into pieces b) bind pathogen pieces to MHC receptors* c) display pathogen on cell membrane d) attract helper T cells* e) helper T cells activate acquired imm. resp.
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http://highered. mheducation
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Natural Killer Cells NK cells vertebrate innate defense.
Attack virus infected cells and cancer cells NOT MHC molecule receptors…just detects changes in cell membrane Produce signal molecules that cause apoptosis
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II aquired/adaptive immunity
A) Humoral Response = B cells make antibodies B) Cell Mediated Response = Cytotoxic T cells defends against: infected cells Cancer cells Transplanted cells
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Antibodies Proteins secreted by differentiated B-cells (plasma cells)
Bind to specific antigen Also called Immunoglobulins (Ig) 1) IgG – give passive immunity to fetus 2) IgA – in secretions, sweat, milk, tears 3) IgE – triggers histamines/ allergic rxns
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Humoral Response = B cells put antibodies in fluid (humor)
1. B cell receptor binds to a Polysaccharide or protein on microbe, pollen or transplanted cell 2. B cell takes in antigen and presents it on MHC surface protein to attract helper T cells 3. Helper T binds to MHC-antigen complex and begins secreting cytokines 4. cytokines induce mitosis in B cell to produce a. plasma cells b. memory B-cells
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Plasma cells make antibodies specific to the antigen that their parent B-cell bound
1.bind & clump viruses/bacteria 2. percipitate antigens dissolved in fluid 3. activate complement proteins Memory B-cells stay in blood stream ready to become activated in secondary immune response.
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Secondary Immune Response
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Cell Mediated Response =fights cancer, infected cells, transplant cells
1. Class I MHC molecule displays antigens that are synthesized inside affected cell 2. Cytotoxic Tcells bind to MHC-antigen complex (CD8 protein ropes them together) 3. Binding makes cytotoxic Tcell secrete: a. perforin (protein, makes holes in membrane) b. enzymes to digest the cell c. signals to cause apoptosis
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More on Helper T Cells Helper T cells Activate by
1. binding C-II MHC-antigen complex on dendritic cells, macrophages, or B-cells 2. Makes cytokines to stimulate a. cytotoxic T cells to become active b. B cells to begin clonal selection….. mitosis to produce plasma & memory cells
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Helper T clonal selection
Activated helper T does mitosis 1 clone divides to make many activated helper T cells The other divides to make memory helper T cells
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Lymphocyte receptor diversity
1 million diff. B cells….10 million diff. T cells When leukocytes differentiate into lymphocytes 1. Recombinase enzymes link 1 V gene segment to 1 J gene segment 2. DNA between selected segments is deleted 3. receptor gene made of V seg + J seg + an intron and a constant segment. 4. that protein makes the receptors light chain 5. all receptors on that cell the same
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Autoimmune disease New lymphocytes are tested to be sure their receptors won’t bind to bodies own cells. Failure to remove self-reactive cells = autoimmune disease
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