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

Seetha M Lakshmi Tamma1, Kun Wook Chung, Tejal Patel

  • 1Department of Biomedical Sciences, C. W. Post Campus, Long Island University, 720 Northern Blvd., Brookville, NY 11548, USA. stamma@liu.edu

Insights

Jacalin and CD28 stimulation activate p38 MAPK in CD4+ T cells, promoting IL-4 secretion and anti-apoptotic protein expression. p38 MAPK inhibition blocks these effects, suggesting its crucial role in T cell activation and survival.

Area of Science:

  • Immunology
  • Cellular Signaling

Background:

  • Jacalin, a CD4+ T cell lectin, induces intracellular phosphorylation and IL-2 secretion.
  • CD28 costimulation with jacalin promotes IL-4 secretion.
  • p38 MAPK is implicated in T cell activation pathways.

Purpose of the Study:

  • To investigate the role of p38 MAPK in CD4+ T cell activation induced by jacalin and CD28 costimulation.
  • To examine the effects of p38 MAPK inhibition on STAT-6, Bcl-2, and Bcl-xL expression.
  • To differentiate the role of p38 MAPK in memory versus naïve T cells.

Main Methods:

  • Stimulation of CD4+ T cells with jacalin and CD28 cross-linking (CD28XL).
  • Inhibition of p38 MAPK using SB203580.
  • Analysis of STAT-6 phosphorylation, Bcl-2 and Bcl-xL expression, and IL-4 secretion.
  • Comparison between normal T cells, T cell blasts, memory T cells, and naïve T cells.

Main Results:

  • Jacalin plus CD28XL induced STAT-6 phosphorylation and Bcl-2/Bcl-xL expression, inhibited by SB203580.
  • CD28XL alone induced p38 MAPK phosphorylation and IL-4 secretion in memory T cells (jacalin blasts).
  • p38 MAPK inhibition significantly reduced STAT-6, Bcl-2, and Bcl-xL expression, an effect not reversed by IL-4.

Conclusions:

  • p38 MAPK plays a significant role in the induction of STAT-6, Bcl-2, and Bcl-xL during CD4+ T cell activation.
  • p38 MAPK activation is critical for IL-4 secretion and expression of anti-apoptotic proteins.
  • p38 MAPK may confer a survival advantage to activated T cells, protecting them from apoptosis.

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