Early preferential stimulation of gamma delta T cells by TNF-alpha.

Journal of immunology (Baltimore, Md. : 1950) (1998-05-30)
M Lahn, H Kalataradi, P Mittelstadt, E Pflum, M Vollmer, C Cady, A Mukasa, A T Vella, D Ikle, R Harbeck, R O'Brien, W Born

Although recent findings indicate that gamma delta T cells influence both early innate and Ag-specific adaptive host responses, it has remained unclear what triggers gamma delta T cell reactivity. Investigating very early T cell activation in mouse and human models of bacterial infection, we measured CD69 expression as an indicator of early cellular activation. Both murine alpha beta and gamma delta T cells responded polyclonally to systemic bacterial infections, and to LPS. However, gamma delta T cells responded more strongly to the bacteria and to LPS. In vitro LPS-stimulated human T cells showed a similar differential response pattern. We identified TNF-alpha as mediator of the early differential T cell activation, and of differential proliferative responses. The stronger response of gamma delta T cells to TNF-alpha was correlated with higher inducible expression levels of TNF-Rp75. Among unstimulated splenocytes, more gamma delta T cells than alpha beta T cells expressed CD44 at high levels. The data suggest that TNF-Rp75 determines the differential T cell reactivity, and that most gamma delta T cells in the normal spleen are present in a presensitized state. As TNF-alpha stimulates activated T cells, it may early preferentially connect gamma delta T cell functions with those of cells that produce this cytokine, including activated innate effector cells and Ag-stimulated T lymphocytes.

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Fluorescein isothiocyanate isomer I–Celite®, suitable for fluorescent labeling techniques
IgG from rat serum, reagent grade, ≥95% (SDS-PAGE), essentially salt-free, lyophilized powder