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p38 MAPK plays a role in IL‐4 synthesis in jacalin plus CD28‐stimulated CD4+ T cells—II
Author(s) -
Tamma Seetha M. Lakshmi,
Chung Kun Wook,
Patel Tejal,
Balan Satya Priya,
Pahwa Savita
Publication year - 2006
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0905513
Subject(s) - jacalin , biology , p38 mitogen activated protein kinases , cd28 , secretion , microbiology and biotechnology , phosphorylation , mapk/erk pathway , t cell , immunology , immune system , endocrinology , lectin
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.