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32 Cards in this Set
- Front
- Back
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define central tolerance
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B and T cell non-response to self during development in bone marrow and thymus
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what is the AIRE gene
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a transcription activator in thymic medullary epithelial cells (MEC) allowing expression of peripheral tissue specific self antigens to test developing T cells against -negative selection, central tolerance
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what happens to T cells with intermediate self affinity at negative selection
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become Treg
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what 3 things are expressed by Treg
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CD4 CD25 Foxp3
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what is the standard mode of peripheral tollerance and what is the other method
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self reactive T cell that has escaped apoptosis at negative selection in the thymus recieves signal 1 as it binds to MHCII with antigen but does not receive signal 2 (from B7 on an APC) so becomes anergic. Alternative method is suppression by Treg
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2 possible methods of Treg action
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1. CTLA-4 on Treg binds to APC B7 inducing production of Kynurenine (immunosuppressive) also B7 is downregulated on APC's so takes away signal 2
2. Treg CD25 competes for IL2 starving CD4 of cytokines also induces production of IL10 (immunosuppressive) |
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what are Tr1 cells and what do they do
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regulatory cells that develop from T0 in the presence of TGFb, similar to Treg bind Il2 and secrete Il10. Tr1 do not express Foxp3
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what cytokine then transcription factor pattern induces Th0 to become Th1 cells and what is Th1 function
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IL12 then T-bet, intracellular pathogen control
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what cytokine then transcription factor pattern induces Th0 to become Th2 cells and what is Th2 function
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Il4 then GATA-3, extracellular pathogen control
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what cytokine then transcription factor pattern induces Th0 to become Treg cells and what is Treg function
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TGFb then Foxp3, anti-inflammatory and suppressive action
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what cytokine then transcription factor pattern induces Th0 to become Th17 cells and what is Th17 function
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TGFb then Il6 then RORyt, plays a roll in DTH and autoimmunity
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what cytokines do Th17 express
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IL17, IL6, TNFa, GM-CSF
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cytokine that promotes Th17 survival and proliferation
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IL23
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where do the cytokines come from that prompt differentiation of Th0
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APC
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function of Th17
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IL17 promotes granulopoesis, activates and attracts neutrophils, GM-CSF promotes bone marrow neutrophil output
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all Th0 derived cells inhibit the proliferation of the other types by prodction of a a specific cytokine which one do Th1 use
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IFN-y
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all Th0 derived cells inhibit the proliferation of the other types by prodction of a a specific cytokine which one do Th2 use
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IL4
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all Th0 derived cells inhibit the proliferation of the other types by prodction of a a specific cytokine which one do Threg use
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TGFb
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all Th0 derived cells inhibit the proliferation of the other types by prodction of a a specific cytokine which one do Th17 use
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IL6
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what is molecular mimicry, classic example
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when there is cross-reactivity of Ab or T cells against microorg Ag's against self epitopes with sequence homolgy. Anti b-haemolytic strep Ab cross react with myocardial cells- rheumatic endocarditis
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2 classes of autoimmune diseases
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organ specific and non-organ specific
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what tissues are affected in rheumatoid arthritis
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primarily synovium but also vasculitis, pericarditis. Systemic autoimmune disease
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general facts about rheumatoid arthritis, succeptibility MHC
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symetrical symptoms, more women, smokers, HLA-DR4
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what is rheumatoid factor
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found in 80% RA sufferers, IgM against Fc of IgG
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pathology of rheumatoid arthritis
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inflammation of synovial membrane, hypertrophy, fibrin, T cell infiltrate, granulation tissue (pannus), immne complexes
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what is pannus
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rheumatoid arthritis granulation tissue in the synovial joints
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cytokines associated with rheumatoid arthritis and what do they do
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TNF family: BAFF and APRIL, promote B cell survival, may inhibit anergy of autoantibodies
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systemic effects of rheumatoid arthritis
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pericarditis, vasculitis, circulating immune complexes, deficient complement due to persistant activation
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rheumatoid arthritis treatment
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NSAIDS, corticosteroids, anti-rheumatics
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systemic lupus erythematosus
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type III hypersensitivity, systemic, immune complexes, autoantibodies agains nucleat antigens
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MS
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CNS autoimmune disease, demyelination plaques, caused by macrophages activated by Th1, chromic, type IV hypersensitivity, genetics nd environment
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myasthenia gravis
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autoAb blocks Ach receptors in post synaptic membrane, gradual depletion of receptors, loss of muscle funtion, wasting
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