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

Wei Li, Carmella D. Whaley, Anna Mondino, Daniel L. Mueller

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)1272-1276
Number of pages5
Issue number5253
Publication statusPublished - Mar 1 1996

ASJC Scopus subject areas

  • General


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