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17 Cards in this Set
- Front
- Back
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why is immunosuppresion required in MHC matched cases
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minor histocompatability antigen mismatches can still cause rejection
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hyperacute rejection is driven by what immune cells
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preformed IgG against MHC I on graft, this requires previous exposure (transplant, transfusion, pregnancy)
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why do host T cells react against graft MHC
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there has been no negative selection against T cells that react to foreign MHC
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4 blood groups, why do we have Ab against other blood groups
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A, B, O, AB. Cross reactivity with bacterial antigens or previous exposure to blood products
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species specific carbohydrate antigens are found on which tissues, why are they important, why do Ab against these exist
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vascular endothelium, hinder xenotransplantation, Ab againt bacterial components cross react with these
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3 types of rejection
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hyper acute, acute, chronic
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hyperacute rejection
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pre-existing Ab's, usually vascular endothelium, usually ABO antigens or MHC I (MHC II little expressed on vascular endothelium), complement activated by Ab's, inflammation, coagulation, fibrinolysis, oedema, neurophil infltration, timescale of minutes/hours
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acute rejection
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timescale of <6 months, T cell mediated, targets MHC and minor histocompatability antigens.
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3 modes of acute rejection
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1. nonspecific inflammatory damage
2. Direct presentation 3. indirect presentation |
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nonspecific inflammatory damage in acute rejection
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transplantation trauma causes inflammation- macrophages, IL1, TNFa, IFNg, attract and activate other immune cells causing tissue damge
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direct presentation in acute rejection
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donor DC present donor antigen to TCR, T cells activated and migrate back to graft
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indirect presentation in acute rejection
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host DC's infiltrate graft, pick up graft antigens (including MHC and B cell antigens) go to lymph nodes, activate T cells, migrate to transplant
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Chronic rejection
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low level rejection over > 6 months cellular and humoral immunity involved
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GVHD
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Donor T cells attack host. Esp in BM transplants and in immunosuppressed patients
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drugs for transplantation
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azothioprine- mitotic inhibitor, slows cell proliferation
corticosteroids- cyclosporine, FK506- inhibit T cell activation by inhibiting IL2 and IL2 receptor transcription (essential for T cell activation) |
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problem of cyclosporine
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nephrotoxic
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future developments for transplants
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blocking T cell signal 2 to induce anergy
DC tolerance, immature DC's induce tolerance so perhaps dose with immature donor DC's Use Treg specific for desired antigens |
