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27 Cards in this Set
- Front
- Back
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T lymphocyte (T cell)
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T cell
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HLA (Human histocompatability Antigen)
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HLA
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MHC (Major Histocompatability Complex)
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MHC
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Hypersensitivity reactions
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1) Type 1- mast cell/ basophil mediated
2) Type 2- direct attack on cells/ tissues by antibodies 3) Type 3- damage secondary to deposition of immune complexes (IgG- Ag) 4) Type 4- T cell / macrophage mediated (delayed type hypersensitivity) |
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Eicosanoids
1) Prostaglandins 2) Leukotrines |
A)
1) 2) |
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CYTOKINES:
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CYTOKINES
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IL1
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CELL SOURCE: macrophages, B cells, NK cells
TARGET CELLS: endothelium, fibroblasts, astrocytes EFFECTS: Lymph activation, mac stimulation, increase leukocytes, endothelium adhesion, acute phase proteins, fevers |
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IL2
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CELL SOURCE: T cells
TARGET CELLS: T cells, NK cells EFFECTS: T cell and NK cell activation and proliferation |
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IL4
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CELL SOURCE: T cells, TH2 cells, mast cells
TARGET CELLS: B cells, T cells EFFECTS: B cell GF, isotype switching to IgE, TH2 differentiation, suppress TH1 cells |
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IL10
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CELL SOURCE: T cells, TH2 cells
TARGET CELLS: TH1 cells EFFECTS: B cell gf, isotype switching to IgA, wosinophil growth |
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IL12
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CELL SOURCE: monocytes, APC
TARGET CELLS: TH1 cells EFFECTS: inhibition of cytokine synthesis and macrophage function |
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TNF alpha
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CELL SOURCE: lymphocytes, macs, mast cells
TARGET CELLS: many cells EFFECTS: proinflammatory, endothelial activation, shock, acute phase proteins, PMN activation |
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IFN gamma
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CELL SOURCE: NK cells, T cells
TARGET CELLS: macs, B cells, endothelium, DCs EFFECTS: increased MHC class II expression, mac activation, IgG class switching, suppress TH2 cells |
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TGF beta
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CELL SOURCE: most cells
TARGET CELLS: most cells EFFECTS: antiviral, increased MHC I expression |
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CHEMOKINES
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CHEMOKINES
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MAST CELLS
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*
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EOSINOPHILS
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*
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MACROPHAGES/ MONOCYTES
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*
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VASCULITIS
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*
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ANAPHYLAXIS
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*
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OPSONIZATION
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*
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Describe TYPE 1 HS.
1) What is anayphylaxis? 2) What happens with the induction of IgE response? 3) What's the difference between primary and secondary mediators? |
* It is mast cell, basophil mediated
1) Can have anyphylaxis: systemic and localized. Examples are asthma, allergic rhinitis 2) Get induction of IgE response after antigen exposure- - TH2 cells as well 3) Primary: preformed mediators Secondary: synthesized mediators |
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Describe Type 2 HS.
1) What diseases are associated with this? (6) 2) What is the mechanism of Type 2 HS? |
* Direct attack on cells. tissues by antibodies
1) Hemolytic anemia, erythroblastosis fatalis, Goodpasture syndrome, Myesthenia gravis, Rheumatic fever, Graves' disease 2) - So get induction of anti- self antibodies, and antibodies bind to self- constituents - Complement fixation/ activation - Tissue lysis/ opsonization/ phagocytosis/ cell- mediated cytotoxicity |
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Describe Type 3 HS.
1) What diseases are associated with this? (5) |
* damage secondary to deposition of immune complexes (IgG- Ag)
1) Glomerulonephritis, serum sickness, polyarteritis nodosa, arthus reaction - Get induction of antibodies and form Ab- Ag complexes - Deposition of copmlexes in tissues or on cells - Complement activation and prod of comp factos - Neutrophil attraction and degranulation and tissue destruction |
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Describe Type 4 HS.
1) What diseases/ reactions are associated with this? (3) 2) What are major characteristics |
* T-cell/ macrophage mediated/ DTH
1) Tuberculin reaction, granuloma formation, contact dermatitis 2) - Must first get sensitization of T cells - Ag processing and presentation - Rechallenge or chronic Ag challenge - Production of cytokines and chemokines - Attract other cells and actication of macs - Form giant cells - Activate CD8 cytotoxic T cells - Form granulomas |
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Describe the significance of Graft/ Tranplant rejection.
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* Combination of HS reaction types 2- 4, but not type 1
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What are the 4 types of transplant rejection?
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1) Ab mediated: hyperacute rejection, thrombosis vessel attack
2) Acute rejection: host becomes sensitized to donor tissue - Cellular and Ab mediated - Get attack on vessels (vasculitis), parenchymal attack and damage 3) Chronic rejection: mixed mechanism, but many macs and T cells and plasma - Extensive and longstanding damage and fibrosis to graft 4) Graft vs. Host disease - Can have acute and chronic - Tranplanted tissue attack the host - See in skin, liver, GI tracts are most affected |
