p38 MAPK plays a role in IL-4 synthesis in jacalin plus CD28-stimulated CD4+ T cells - II

Seetha M.Lakshmi Tamma, Wook Chung Kun, Tejal Patel, Satya Priya Balan, Savita Pahwa

Research output: Contribution to journalArticle

9 Scopus citations

Abstract

We have previously shown that jacalin, a CD4+ T cell lectin, induces phosphorylation of intracellular events, moderate levels of interleukin (IL)-2 secretion. We have also shown that in the presence of CD28 costimulation, jacalin induces IL-4 secretion. In the present study, we showed that stimulation of normal CD4+ T cells with jacalin plus CD28 cross-linking (CD28XL) resulted in phosphorylation of signal transducer and activator of transcription (STAT)-6 and expression of Bcl-2 and Bcl-xL, which were inhibited significantly when cells were cultured in the presence of the p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580. We further generated jacalin-induced CD4+ T cell blasts, examined the effects of CD28XL, and observed enhanced up-regulation of p38 and activation of STAT-6, Bcl-2, and Bcl-xL. Engagement of CD28 alone induced a marked degree of phosphorylation of p38 MAPK and IL-4 secretion in memory T cells (jacalin blasts), whereas in naïve T cells, jacalin plus CD28XL was required to induce these molecules. Incubation of cells with p38 inhibitor prior to CD28XL resulted in down-modulation of all these molecules. Further treatment with IL-4 has not reversed this trend. Our studies imply that p38 MAPK may play an important role in induction of these molecules and a putative role in protecting cells from undergoing apoptosis.

Original languageEnglish (US)
Pages (from-to)1339-1347
Number of pages9
JournalJournal of Leukocyte Biology
Volume79
Issue number6
DOIs
StatePublished - Jun 1 2006

Keywords

  • Bcl-2
  • Bcl-xL
  • STAT-6

ASJC Scopus subject areas

  • Cell Biology

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