Abstract
Abstract Cell death by programmed necrosis (also known as caspase-independent cell death or necroptosis) is characterized by rapid loss of plasma membrane integrity prior to the exposure of phagocytic signal. The release of endogenous "danger signals" from necrotic cells trigger inflammation and may have important physiological and pathological consequences in immune responses, inflammatory diseases and cancer growth. However, the role of programmed necrosis in immune responses and inflammation has not been adequately tested, in part because the molecular pathway that regulates programmed necrosis was ill-defined. The serine/threonine kinase RIP1 plays crucial role in programmed necrosis induced by TNF and other stimuli. We performed a RNA interference (RNAi) screen to identify downstream regulators of RIP1-dependent programmed and identified RIP3 to be another kinase critically required for TNF-induced programmed necrosis. In order to test the role of programmed necrosis in inflammation and anti-viral immune responses, we infected RIP3-deficient mice with vaccinia virus and found that the RIP3-deficient mice were highly sensitive to vaccinia virus infections. The details of these studies and the physiological implications of programmed necrosis will be discussed.
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