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18 Cards in this Set
- Front
- Back
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List the innate mechanisms used for 1st line defense |
Mechanical barriers Peristalsis of GIT Expulsion effects of mucociliary escalator Washing effects of saliva, urine, tears Complement proteins Antimicrobial agents in secretions (lysozyme, defensis, surfactants A + D) Neutrophils + NK cells Toll - like receptors Unfavourable ph of skin + stomach |
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Which 2 diseases re associated with the mucociliary escalator? |
Cystic fibrosis Primary ciliary dyskinesia |
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What are the functions of vascular endothelium? |
Vascular tone Vascular repair Coagulation Angiogenesis Blood - tissue permeability Chemotaxis + adhesion |
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Explain the adhesive interactions between leukocytes and vascular endothelium |
Tethering + rolling (Physical + E selection --> L selectin) Chemo attractant binding B integrins --> VCAM + ICAM = transendothelial migration |
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What synthesis does the interaction between epithelial and phagocytosis TLR and microbes result in? |
a + B defensis a + B interferons Proinflammatory cytokines (IL1,6,8 + TNFa) Histamine |
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What are key events in generating proinflammatory polypeptides? |
Histamine induced increased vascular permeability Mannan-binding lectin synthesis by IL6-activated hepatocytes Complement activation by C3b and MBL |
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How can MBL and C3b distinguish between self and non self antigens? |
MBL = mannose C3b = low silicone acid |
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What are the functions of the various complement components? |
C3a + C5a = chemotactic + anaphylatoxic C3b + C3bi = opsonins C3e = BM activator --> NP C5b,6,7,8,9 = cell wall attack compkex |
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How do phagocytes achieve intracellular killing? |
1) Preformed granule-derived antimicrobial polypeptides Lactoferrin Lysozyme a defensin Bactericidal permeability increasing protein Proteolytic enzymes 2) Newly synthesised antimicrobial oxidants Superoxide Hydrogen peroxide Hydrochlorous acid Nitrogen oxide |
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Describe chemotaxis |
Resting bv = reduced ECAMs Endothelium activated (histamine, TNF-a, IL1) + chemoattractants (IL8, N-formylated polypeptides, C3a + C5a) Increased ECAM + NCAM expression Widening gaps + tighter binding Transendothelial migration = accumulate = chemoattractants (IL8, leukotriene B4, PG-E) |
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Describe phagocytosis |
1. Opsonisation (C3b + C3bi =neutralisation) 2. Immune adherence (C3b = CR1; C3bi = CR3) 3. Ingestion |
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Why are dendritic cells essential for primary immune response? |
High expression of HLA II Many co-stimulatory molecules Retinaculum Ag/HLA II complex for long periods Bind to CO2 and CD8 |
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Describe 4 was in which innate and adaptive immunity interact |
Classic complement pathway activation Cytokines/ chemokines/ histamine = recruit T and B cells AP + delivery Orchestrate T cell differentiation (TH1, TH2) |
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Describe how the body controls inflammatory and immune responses |
Up-regulation of anti - oxidative enzymes Synthesis of anti - inflammatory acute phase reactants Clearance of Ag Anti-inflammatory cytokines Synthesis of cortisol and adrenaline Expression of CTLA-4 Compliment inhibitors Anti-inflammatory/ immunosuppressive chemotherapy |
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Which chemotherapy can be used to control immune/ inflammatory responses? |
Corticosteroids Cyclosporin A Methotrexate, Chloroquin, Sulfasalazine Cytotoxic agents Monoclonal AB to TNF-a |
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How are the elderly's immune systems affected? |
Innate: Reduced TLR Reduced chemotaxis, phagocytosis and NP antimicrobial activity Reduced NK protection Adaptive: Thymic atrophy =/= T cell maturation Limited capacity of T and B cells to replicate |
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What are the consequences of the elderly being immune compromised? |
HIV Bacterial infections Recitation of dormant TB / Herpes Zester Severe pneumococcal, influenza, RSV infections Reduced pneumococcal nd influenza vaccine efficacy Autoimmune diseases + malignancies |
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How do tumour cells evade the immune system? |
Weakly immunogenic Produce immunosuppressive factors Down-regulate HLA I expression |
