Discussion in 'MRCS Forum' started by bronzy, Nov 10, 2007.

  1. bronzy

    bronzy Guest

    useful for understanding...
    A plausible mechanism for ANCA vasculitis is:

    Neutrophil release of PR3 and MPO (e.g., in the setting of infections) incites ANCA formation in a susceptible host.Some underlying disorder (e.g., infection, endotoxin exposure, etc.) elicits inflammatory cytokines, such as TNF, that result in surface expression of PR3 and MPO on neutrophils and other cell types.ANCAs react with these cytokine-primed cells and either cause direct injury (e.g., to endothelium) or induce activation (e.g., in neutrophils).ANCA-activated neutrophils degranulate and also cause injury by the release of reactive oxygen species, engendering EC toxicity and other direct tissue injury.

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