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Explain the difference between direct and indirectallorecognition regarding tissue transplantation
Direct
Donor DCs
activate T cells
alloreactive CTLs
Indirect
graft cells ingested by host DCs
MHC present to T
alloreactive T cells
what are the different types of graft rejections and what is involved in each type?
1 - HYPER ACUTE
within minutes, thrombus developed in graft vessels leading to ichaemia
mediated by circulating Abs specific for graft endothelial cells
2 - ACUTE
days/weeks, T (CD4/8 Allo) and Ab mediated response specific for graft
Classical complement pathway
3 - Chronic
months/years later, fibrosis of graft (narrowing BVs) T cells reacting against allo Ag ->cytokines -> fibroblasts
What are immune responses to tumours?
Tumour cell recognised by mutated self protiens, products of oncogenes/mutated suppressor genes, over expressed self protiens, products of onconic virus
DC phagocytoses tumour Ag
activates Ag specific CD8+ CTL in lymph node
Migration of CTL to tumour
CTL kills tumour cell
What are some tumour evasion mechanisms from the immune response?
Failure to produce tumour Ag
Mutations in MHC genes needed for Ag processing
Production of immunosuppressive protiens (TGF Beta) and inhibitory cell surface receptors (ligands, PD1)
what are some strategies for enhancing antitumour responses?
1. passive immunity
transfer tumour specific T cells or Ab into patient in combination with chemotherapy
(take T cells/Ab, prolif, put back)
2. Checkpoint blockade: active immunity enhanced by blockade of inhib molecules
-vaccination of tumour Ag (take DCs, show cancer in culture, put polyclonal DCs back)
-block cancer inhib signals for lymphocytes
(PD1 + CTLA4 for melanoma FDA approved!)
How does someone typically develop an autoimmune disorder?
inheritance of susceptibility genes + environmental triggers
What are the mechanisms of microbes that can lead to autoimmunity?
1.infection -> innate response -> increase in cytokines and costim from APC -> APC stimulate self reactive T cell -> autoimmunity
2. Peptide Ag are similar to (or can cross react with) self Ag
3. innate immune response alters structure of self Ag (eg rheumatoid arthritis)
acute and chronic response to bacteria causes enzymatic conversion in self protiens, recognised as non self
(also infection may lead to exposure of self Ag that are usually sequested from immune system (eg eye/testes trauma leading to exposure))
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