Abstract

Several studies examined the mechanism responsible for T-cell death during the contraction phase of an antiviral immune response focusing on the relative contribution of different death receptors and individual BH3-only proteins. These studies identified a dominant role for Bim1 with auxiliary roles for Puma2 in acute infection. In the case of chronic infections, Bim cooperates with Bid to constrain the T-cell response3 in concert with death receptor signals to control unrestrained inflammation and to preclude autoimmunity.4

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