Published online before print March 22, 2006

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(Journal of Leukocyte Biology. 2006;79:1339-1347.)
© 2006 by Society for Leukocyte Biology

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

Seetha M. Lakshmi Tamma^*,1, Kun Wook Chung^*, Tejal Patel^*, Satya Priya Balan^* and Savita Pahwa

^* Department of Biomedical Sciences, C. W. Post Campus, Long Island University, Brookville, New York; and
University of Miami, School of Medicine, Microbiology and Immunology, Florida

¹Correspondence: Department of Biomedical Sciences, School of Health Professions and Nursing, C. W. Post Campus, Long Island University, 720 Northern Blvd., Brookville, NY 11548. E-mail: stamma{at}liu.edu

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.

Key Words: STAT-6 • Bcl-2 • Bcl-xL

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