Fas-Fas ligand interactions are essential for the binding to and killing of activated macrophages by gamma delta T cells

Dalton, Jane E., Howell, Gareth, Pearson, Jayne, Scott, Phillip and Carding, Simon R. (2004) Fas-Fas ligand interactions are essential for the binding to and killing of activated macrophages by gamma delta T cells. Journal of Immunology, 173 (6). pp. 3660-3667. ISSN 0022-1767

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Abstract

Gammadelta 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 Vgamma1/Vdelta6.3 subset of gammadelta T cells, which have the ability to kill activated macrophages following infection with Listeria monocytogenes (Lm). However, it is not known how gammadelta T cell macrophage cytocidal activity is regulated, or what effector mechanisms gammadelta T cells use to kill activated macrophages. Using a macrophage-T cell coculture system in which peritoneal macrophages from naive or Lm-infected TCRdelta-/- mice were incubated with splenocytes from wild-type and Fas ligand (FasL)-deficient mice (gld), the ability of Vgamma1 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 Vgamma1 T cells. In addition, confocal microscopy showed that Fas and the TCR colocalized on Vgamma1 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 Vgamma1 T cells with activated macrophages and their elimination during the resolution stage of pathogen-induced immune responses.

Item Type:	Article
Faculty \ School:	Faculty of Medicine and Health Sciences > Norwich Medical School
UEA Research Groups:	Faculty of Medicine and Health Sciences > Research Groups > Gastroenterology and Gut Biology
Depositing User:	Rhiannon Harvey
Date Deposited:	14 Jul 2011 11:12
Last Modified:	06 Sep 2023 11:30
URI:	https://ueaeprints.uea.ac.uk/id/eprint/33718
DOI:	10.4049/jimmunol.173.6.3660

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