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γδ  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  γδ  T cells responds to nonpeptidic antigens, such as isopentylpyrophosphate (IPP), a metabolite in the mevalonate pathway for both eukaryote and prokaryote cells. IPP-primed  γδ  T cells significantly augment the inflammatory response mediated by monocytes and  αβ  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  γδ  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  γδ  T cells may serve as influential modulators of both endogenous and exogenous stress stimuli.

mediators of inflammation

Linking Innate and Adaptive Immunity: Human V<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>γ</mml:mi></mml:math>9V<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>δ</mml:mi></mml:math>2 T Cells Enhance CD40 Expression and HMGB-1 Secretion

Linking Innate and Adaptive Immunity: Human Vγ9Vδ2 T Cells Enhance CD40 Expression and HMGB-1 Secretion