Ralph C. Budd

TL;DR: Evidence is provided that FLIP is not simply an inhibitor of death-receptor-induced apoptosis but that it also mediates the activation of NF-kappaB and Erk by virtue of its capacity to recruit adaptor proteins involved in these signaling pathways.

TL;DR: It is reported here that CD3-induced proliferation and interleukin 2 production by human T cells are blocked by inhibitors of caspase activity, extending the role of death receptors to the promotion of T cell growth in a casp enzyme-dependent manner.

TL;DR: Evidence suggests that CD95 mediates not only apoptosis but also diverse nonapoptotic functions depending on the tissue and the conditions.

TL;DR: Two major patterns of cytokine synthesis were initially recognized, and these two patterns appear to correlate with the induction of delayed-type hypersensitivity and help for antibody synthesis, thus providing a possible explanation for the separate and often reciprocal regulation of these two responses.

TL;DR: Insight gained from studies indicates that cFLIP and caspase-8 form a heterodimer that ultimately links T-cell-receptor signalling to activation of nuclear factor-κB through a complex that includes B-cell lymphoma 10 (BCL-10), mucosa-associated-lymphoid-tissue lymphoma-translocation gene 1 (MALT1) and receptor-interacting protein 1 (RIP1).