Comment in:

Science. 1996 Mar 1;271(5253):1234.

Blocked signal transduction to the ERK and JNK protein kinases in anergic CD4+ T cells.

Department of Medicine, University of Minnesota Medical School, Minneapolis 55455, USA.

T cells activated by antigen receptor stimulation in the absence of accessory cell-derived costimulatory signals lose the capacity to synthesize the growth factor interleukin-2 (IL-2), a state called clonal anergy. An analysis of CD3- and CD28-induced signal transduction revealed reduced ERK and JNK enzyme activities in murine anergic T cells. The amounts of ERK and JNK proteins were unchanged, and the kinases could be fully activated in the presence of phorbol 12-myristate 13-acetate. Dephosphorylation of the calcineurin substrate NFATp (preexisting nuclear factor of activated T cells) also remained inducible. These results suggest that a specific block in the activation of ERK and JNK contributes to defective IL-2 production in clonal anergy.

PMID: 8638107 [PubMed - indexed for MEDLINE]