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The Interaction of T Cells with Activated Macrophages Is a Property of the V1 Subset ¹

Jane E. Dalton^*, Jayne Pearson^*, Phillip Scott and Simon R. Carding^2,*

^* School of Biochemistry and Molecular Biology, University of Leeds, Leeds, United Kingdom; and Department of Pathobiology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA 19104

Immunoregulation is an emerging paradigm of T cell function. The mechanisms by which T cells mediate this function, however, are not clear. Studies have identified a direct role for T cells in resolving the host immune response to infection, by eliminating populations of activated macrophages. The aim of this study was to identify macrophage-reactive T cells and establish the requirements/outcomes of macrophage- T cell interactions during the immune response to the intracellular bacterium, Listeria monocytogenes (Lm). Using a macrophage-T cell coculture system in which peritoneal macrophages from naive or Lm-infected TCR^-/- mice were incubated with splenocytes from naive and Lm-infected / T cell-deficient and wild-type mice, the ability to bind macrophages was shown to be restricted to T cells and the GV5S1 (V1) subset of T cells. Macrophage adherence resulted in a 4- to 10-fold enrichment of V1⁺ T cells. Enrichment of V1 T cells was dependent upon the activation status of macrophages, but independent of the activation status of T cells. V1 T cells were cytotoxic for activated macrophages with both the binding to and killing of macrophages being TCR dependent because anti-TCR Abs inhibited both V1 binding and killing activities. These studies establish the identity of macrophage cytotoxic T cells, the conditions under which this interaction occurs, and the outcome of this interaction. These findings are concordant with the involvement of V1 T cells in macrophage homeostasis during the resolution of pathogen-mediated immune responses.

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