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7 Cards in this Set

  • Front
  • Back

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))