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9 Cards in this Set
- Front
- Back
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What is the difference between auto and allo antibodies? |
Autoantibodies - react with antigens on own RBCS Alloantibodies - react with antigens not on own RBCS but from other humans - transplantation |
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What is alloimmunity caused by? |
Highly pleomorphic/polygenic genes - genes of the MHC - recognised by T lympho and mono. HLA DQ/DP/DR/A/B/C |
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What are the 3 types of rejection? |
Acute - Antigen specific Th1onto MHC-II -> IL-2 -> CD8+ onto MHC-I complexes - days - weeks Hyperacute - antibody mediated IgM or previous antibodies activating complement. Neutro, phago and NK involved. Minutes to hours. Chronic -Alloantibody and cytokine production, graft endothelial damage and fibrosis. Months to years |
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What is the difference between direct and indirect allorecognition? |
Direct - just Th1 -> CD8+, both MHC-II and MHC-I Indirect - shed antigens -> autoAPC - > CD4+ -> CD8+ only MHC-I involved |
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What are the main mechanisms of tolerance in adaptive immunity? |
Central and peripheral deletion Switching cells off - anergic Active regulation i.e. Treg17 CD4+CD25+ |
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What occurs post-thymectomy after birth? |
T cell depletion -> autoimmunity e.g. gastritis, thryoiditis, oophritis, diabetes Transfer of CD4+ that express CD25 prevents autoimmunity. |
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When does a T cell become anergic? |
When it recognises an antigen but is not activated. |
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How does an APC activate the Th lymphocyte? |
HLA class II -> T cell receptor binding with the antigen expressed + B7 -> CD28 on T cell binding Both signals activate T cell and cause cytokine gene activation -> IL-2 -> activate other T cells. |
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What is the main complement molecule in alloimmunity? |
C4d - covalent bonds with thioester groups on endothelial cell surfaces and matrix components -> acute cellular and humoral rejection |
