Bim regulates alloimmune-mediated vascular injury through effects on T-cell activation and death.

ABSTRACT:

Objective

Bim is a proapoptotic Bcl-2 protein known to downregulate immune responses and to also be required for antigen-induced T-cell activation. However, it is not known how the effect of Bim on these offsetting processes determines the outcome of allogeneic immune responses. We have defined the role of Bim in regulating alloantigen-driven T-cell responses in a model of vascular rejection.

Approach and results

Bim was required for proliferation of CD4 and CD8 T cells, and for interleukin-2 production, in T cells stimulated with alloantigen in vitro. Moreover, a partial reduction in Bim expression was sufficient to attenuate T-cell activation, whereas a complete elimination of Bim was required to prevent CD4 T-cell death in response to cytokine withdrawl. When alloimmune-m

SUBMITTER: von Rossum A 

PROVIDER: S-EPMC4097606 | biostudies-literature | 2014 Jun

REPOSITORIES: biostudies-literature