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T Cells by TNF-
1
*
National Jewish Medical and Research Center, Denver, CO 80206;
Division of Biostatistics and
Department of Immunology, University of Colorado Health Sciences Center, Denver, CO 80262;
§
Department of Microbiology, Oregon State University, Corvallis, OR 97331; and
¶
Littman-Hart Information Division, Englewood, CO 80111
Although recent findings indicate that 
T cells influence
both early innate and Ag-specific adaptive host responses, it has
remained unclear what triggers 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 
ß and T cells responded
polyclonally to systemic bacterial infections, and to LPS. However,
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- as mediator of the early
differential T cell activation, and of differential proliferative
responses. The stronger response of T cells to TNF- was
correlated with higher inducible expression levels of TNF-Rp75.
Among unstimulated splenocytes, more T cells than ß T cells
expressed CD44 at high levels. The data suggest that TNF-Rp75
determines the differential T cell reactivity, and that most T
cells in the normal spleen are present in a presensitized state. As
TNF- stimulates activated T cells, it may early preferentially
connect 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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