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Mediators of Inflammation
Volume 2009 (2009), Article ID 819408, 9 pages
Research Article

Linking Innate and Adaptive Immunity: Human V 9V 2 T Cells Enhance CD40 Expression and HMGB-1 Secretion

Division of Infectious Diseases, Departments of Medicine, Microbiology and Immunology, University of British Columbia and Vancouver Hospital Coastal Health Research Institute, Vancouver, BC, Canada V5Z 3J5

Received 23 June 2009; Accepted 17 July 2009

Academic Editor: Magdalena Klink

Copyright © 2009 Shirin Kalyan and Anthony W. Chow. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


T cells play an important role in regulating the immune response to stress stimuli; however, the mean by which these innate lymphocytes fulfill this function remains poorly defined. The main subset of human peripheral blood T cells responds to nonpeptidic antigens, such as isopentylpyrophosphate (IPP), a metabolite in the mevalonate pathway for both eukaryote and prokaryote cells. IPP-primed T cells significantly augment the inflammatory response mediated by monocytes and T cells to TSST-1, the staphylococcal superantigen that is the major causative agent of toxic shock syndrome. Here we show that the small pool of activated peripheral T cells induces an early upregulation of CD40 on monocytes and the local release of High Mobility Group Box-1 (HMGB-1), the molecule designated as the late mediator of systemic inflammation. This finding provides a new basis for how T cells may serve as influential modulators of both endogenous and exogenous stress stimuli.