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| Question | Answer |
| MAC-membrane attack complex | formed by C9 polymers |
| mechanism of host defense against intracellular infection by mycobacteria | macrophage activation |
| how does macrophage activation work | 1.peptides of organisms hidden in phagosomes of macrophages are displayed. 2. recognised by TH1 cells. 3. TH1 cells release proteins and cytokines. 4. macrophage stimulated to eliminate pathogen |
| neutrophils are one of first cells on scene and have granules containing.. | toxic substances that kill or inhibit growth of bact/fungi |
| dendritic cells are | phagocytic cells in contact with external environment, mainly the skin (Langerhans ), and the inner mucosal lining of the nose, lungs, stomach and intestines. |
| When activated by a pathogen encounter, basophils release | histamine. important in defense against parasites, and play a role in allergic reactions (such as asthma). |
| Upon activation, eosinophils secrete a range of | highly toxic proteins and free radicals highly effective in killing bacteria and parasites, but also resp for tissue damage during allergic reactions. Activation and toxin release therefore tightly regulated |
| Natural killer cells, or NK cells, are a component of the innate immune system which does not | directly attack invading microbes |
| γδ T (gamma/delta) T cells | on border between innate and adaptive |
| gamma delta T cells may also be considered part of the innate immune system where | a restricted TCR or NK receptors may be used as a pattern recognition receptor. |
| the plasma proteins of complement work together to... | 1. recruit inflammatory cells. 2. "tag" pathogens for opsonisation. 3. forming MAC 4. rid body of neutralised antigen-antibody complexes. |
| when activated, mast cells | rapidly release characteristic granules, rich in histamine and heparin, along with various hormonal mediators, and chemokines |
| Killing bacteria via phagocytosis | 1. Chemotaxis 2. Adherence through pamp recognition 3. Membrane activation 4. Initiation of phagocytosis 5. Phagosome formation 6. Fusion 7. Kill/ digest 8. Release degradation products |
| Some bacteria grow inside macrophages and are not killed | Chlamydia, mycobacterium, listeria |
| 4 Consequences of complement activation | 1. Lysis 2. Opsonisation 3. Inflammation 4. Clearance |
| 5 Symptoms of inflammation | Redness, heat, pain, swelling, loss of function |
| 3 inflammatory stages | 1. Vasodilation and increased permeability of blood vessels. 2. Phagocyte migration and phagocytosis 3. Tissue repair |
| Vasodilation and increased permeability | Vasodilation:increased blood flow = redness and heat. Increased permeability = swelling |
| Fever | 1. Caused by release of interleukin-1 2. Increase in production of T lymphocytes. 3. Intensifies effect of interferon 4. Inhibits growth of organisms by decreasing iron 5. Helps body tissues repair |
| Characteristics of innate immunity | Responds rapidly. Poly specific. No memory |
| Cells of innate immunity | Phagocytes (pmns and macrophages) NK cells, mast cells, dendritic cells |
| Molecules of innate immunity | Cytokines, complement, acute phase proteins |
| Complement is a | Series of plasma proteins in blood, has important role in inflammation, three stages |
| Three stages of complement | 1. Initial activation stage (anitgen) 2. Amplification stage (generation of enzymes and fragments) 3. Lytic stage (assembly of components to form MAC) |
| Three pathways of complement activation | Alternative, classical and lectin |
| Alternative pathway | First evolutionary . Activated on contact with antigen. does not require antibody. |
| Classical pathway | Best understood. Triggered by binding of antibody to antigen.7-10 days to become fully active |
| Lectin pathway | Activation by certain microbial antigens- same as classical w/o abs |
| monocytes and macrophages are, have, do | 1.Highly phagocytic, 2.large lysosomes, 3.phagocytosis of microbes, 4.clearance of own cells and debris |
| Macrophage life cycle | Pluripotent stem cell-->promonocyte --> stromal macrophage or blood monocytes. Blood monocytes --> peri vascular or tissue macrophage. |
| Granulocytes | Neutrophils, basophils and eosinophils |
| Neutrophils | 60-70% all leukocytes, highly phagocytic, activated in initial stages of infection |
| PAMPs | Pathogen associated membrane patterns |
| Phagocytes have what to recognise PAMPs | PRRs - pattern recognition receptors |
| Toll like receptors are found on | mammalian mononuclear phagocytes , dendritic cells and B cells. |
| How are toll like receptors designated and what do they recognise | TLR 1-9. Each receptor recognises a small range of conserved molecules from a group of pathogens |
| What do TLRs recognise from gram negative bacteria | Lipopolysaccharide (lps) |
| What to TLRs recognise from gram positive bacteria | Peptidoglycan |
| The binding of PRR to TLRs leads to the production of | Inflammatory cytokines |
| Structure of a TLR: outside | LRR (leucine rich repeat) domain 24-29 amino acid motif xxLxLxx |
| Structure of a TLR: inside | TIR (toll/IL-1) domain (200 amino acids) signalling box |
| Mannose receptors on myeloid cells : | Eight C Type lection domains bind to mannosyl/fucosyl residues and a terminal lectin domain that binds to sulphated carbohydrate groups |
| Scavenger receptors on macrophages, dendritic cells and some endothelial cells: | Structurally diverse group of receptors. Bind to bacteria and help macrophages phagocytise. Also promote clearance of apoptotic cells. |
| Secretion types | Eyes, ears, mouth, skin, stomach |
| Phagocytic barriers to infection | Microglia, lymph nodes, macrophages alveolar:, pleural cavity, splenic, synovial fluid, kupffer cells, blood monocyte precursors, |
| Monocytes/macrophages: dual function assists... | with both innate and adaptive immunity |
| Myeloid cells active in innate immunity (6) | 1. Macrophage 2. Dendritic cells 3. Neutrophils 4. Eosinophils 5. Basophils 6. Mast cells |
| First line of innate defence | Mechanical barriers: skin, mucus, cilia, fatty acids, stomach acid, gut flora, secretions |
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