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(PMN – polymorphonuclear leukocytes) Phagocytic Migrate to damaged/infected areas in blood Granulocyte |
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Anti-parasitic Limit inflammatory response Granulocyte |
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Inflammatory response Granulocyte |
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Agranulocytes Specific immune response Two general types T cells: responsible for cell mediated immunity B cells: responsible for humoral response Agranulocytes |
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Immature: leave blood and differentiate into macrophages or dendritic cells Agranulocytes |
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Inflammatory response Widely distributed |
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Phagocytic Involved in specific immunity and other responses |
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Involved in specific immunity. from monocytes |
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Natural Killer (NK) Cells |
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NK cells destroy your cells if they loose their MHC class I proteins. perforin and granzymes |
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Major histocompatibility complex I When do cells loose MHC class I molecules? Some malignant cells. Result of some intracellular infections. |
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System of vein-like vessels that return fluid that leaks from blood capillaries back to the circulatory system |
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vessels expansions filled with lymphocytes and macrophages respond to foreign cells, molecules, etc in lymph |
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Skin Associated Lymphatic Tissue |
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Neutrophils (PMNs) Macrophages (Dendritic cells) |
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built by your cells. Antibodies Activated complement proteins |
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pathogen-associated molecular patterns
Membrane protein receptors of phagocyte bind to these target molecules: LPS, Peptidoglycan, etc
Results in Phagocytosis or Production and expression of cytokines |
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Toll-Like Receptors Receptor proteins of phagocytes that bind to PAMPs. |
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taken into phagosome. Killed and Digested Reactive Oxygen compounds H2O2, O2-, etc Chemicals and enzymes in lysosomes. |
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After phagocytosis, fragments of digested molecules attached to MHC (I and II) proteins and displayed on surface |
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Antigen Antibody complexes activate C1, which splits C2 and C4 into C2a, C2b, C4a and C4b. C2a and C4b bind together and activate C3. |
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mannose binding lectin secreted from liver as a result of activated macrophages binds to carbohydrate (mannose) found in many bacterial cell walls and the envelopes of some viruses bound lectin splits C2 and C4 into C2a, C2b, C4a and C4b. C2a and C4b bind together and activate C3. |
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Cytokine secreted by viral infected cells Stimulate production of AVPs (antiviral proteins) in nearby cells Inhibits replication of viral nucleic acids in these cells |
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Antimicrobial Peptides: produced by host cells in response to contact with certain microbial chemicals Inhibit cell wall synthesis Enhance inflammation Counteract LPS |
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Lipopolysaccharides act as endotoxins |
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Iron Binding Proteins blood and tissue fluids Cytokines from macrophages increase their production during infection. |
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Iron Binding Proteins milk, saliva, mucus Cytokines from macrophages increase their production during infection. |
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C5b+C6+C7+C8+C9= Membrane attack complex! perforates cell membrane |
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opsonization (Complement) |
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C3b Enhancement of phagocytosis by coating with C3b, near by cytolysis |
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C5a, C3a Mast cells and/or basophils release histamine, Blood vessel permeability increases + chemotaxic attraction of phagocytes
redness, swelling, pain, heat
chemicals that stimulate pain receptors leukotrienes – attract phagocytes (chemotaxis) |
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C3 combines with B, D, and P factors on microbe, which makes C3 split |
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Inflamation mechanism:
vasodilation increases blood flow to area Increased delivery of leukocytes and chemical factors that inhibit infection. Clotting factors, complement, etc. heating inhibit microbes and more efficient defenses edema (swelling) More fluid into lymphatic vessels |
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