External and Internal Defenses Immune System Chapter 35 External and Internal Defenses

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

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

* 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)

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

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

I. Innate Immunity A) Antimicrobial proteins B) inflammatory response C) Systemic response D) Phagocytic Cells E) Natural Killer Cells

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)

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

C) Systemic Response Widespread response Increased WBC production Fever – facilitates phagocytosis Septic shock – bacterial infection causes high fever low bp may cause death

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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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

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

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

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

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.

Secondary Immune Response

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) http://highered.mheducation.com/sites/0072495855/student_view0/chapter24/animation__cytotoxic_t-cell_activity_against_target_cells__quiz_1_.html 3. Binding makes cytotoxic Tcell secrete: a. perforin (protein, makes holes in membrane) b. enzymes to digest the cell c. signals to cause apoptosis

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

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

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

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