Journal of Leukocyte Biology Myeloid cells, immune suppression, tumor immunology
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A more recent version of this article appeared on June 1, 2008

Published online before print March 25, 2008
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.1007686

Received for publication October 11, 2007.
Revised February 20, 2008.
Accepted for publication February 25, 2008.

Article

SEB-induced signaling in macrophages leads to biphasic TNF-{alpha}

Aslam Ali Khan , Sunil Martin , and Bhaskar Saha @

National Centre for Cell Science, Ganeshkhind, Pune, India

@ To whom correspondence should be addressed. E-mail: sahab{at}nccs.res.in.


  Abstract

APCs express MHC-II molecules. Binding of enterotoxins to MHC-II generates a signal resulting in the production of TNF-{alpha} that mediates toxic shock syndrome. However, the signaling events that lead to TNF-{alpha} production in macrophages are not well understood. We, for the first time, demonstrate that binding of staphylococcal enterotoxin B to MHC-II results in activation of TNF-{alpha}-converting enzyme, epidermal growth factor receptor, p38MAPK, and NF-{kappa}B inducing biphasic TNF-{alpha} production. Paraformaldehyde-fixed, peptide-specific T cells also activate MHC-II signaling and TNF-{alpha} induction in peptide-pulsed macrophages. Our results reveal a novel MHC-II signaling and bidirectional macrophage-T cell interaction regulating macrophage functions. This knowledge may help to develop novel, macrophage-directed, therapeutic strategies.

Key Words: MHC class-II signaling • staphylococcal enterotoxin B • superantigen • APC-T cell interaction






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