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Fas-Fas Ligand Interactions Are Essential for the Binding to and Killing of Activated Macrophages by T Cells

Jane E. Dalton^*, Gareth Howell^*, Jayne Pearson^*, Phillip Scott and Simon R. Carding^1,*

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

T cells have a direct role in resolving the host immune response to infection by eliminating populations of activated macrophages. Macrophage reactivity resides within the V1/V6.3 subset of T cells, which have the ability to kill activated macrophages following infection with Listeria monocytogenes (Lm). However, it is not known how T cell macrophage cytocidal activity is regulated, or what effector mechanisms T cells use to kill activated macrophages. Using a macrophage-T cell coculture system in which peritoneal macrophages from naive or Lm-infected TCR^–/– mice were incubated with splenocytes from wild-type and Fas ligand (FasL)-deficient mice (gld), the ability of V1 T cells to bind macrophages was shown to be dependent upon Fas-FasL interactions. Combinations of anti-TCR and FasL Abs completely abolished binding to and killing of activated macrophages by V1 T cells. In addition, confocal microscopy showed that Fas and the TCR colocalized on V1 T cells at points of contact with macrophages. Collectively, these studies identify an accessory or coreceptor-like function for Fas-FasL that is essential for the interaction of V1 T cells with activated macrophages and their elimination during the resolution stage of pathogen-induced immune responses.

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