Reports

Blocked Signal Transduction to the ERK and JNK Protein Kinases in Anergic CD4+ T Cells

+ See all authors and affiliations

Science  01 Mar 1996:
Vol. 271, Issue 5253, pp. 1272-1276
DOI: 10.1126/science.271.5253.1272

Abstract

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.