FADD and the NF-κB family member Bcl-3 regulate complementary pathways to control T-cell survival and proliferation

Abstract

Fas-associated protein with death domain/mediator of receptor induced toxicity (FADD/MORT1) was first described as a transducer of death receptor signalling but was later recognized also to be important for proliferation of T cells. B-cell lymphoma 3 (Bcl-3) is a relatively little understood member of the nuclear factor (NF)-κB family of transcription factors. We recently found that Bcl-3 is up-regulated in T cells from mice where FADD function is blocked by a dominant negative transgene (FADD-DN). To understand the importance of this, we generated FADD-DN/bcl-3-/- mice. Here, we report that T cells from these mice show massive cell death and severely reduced proliferation in response to T-c..