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CUTTING EDGE |
,
*
Laboratoire d’Immunologie Cellulaire, Unité Mixte de Recherche 7627, Centre National de la Recherche Scientifique Bâtiment CERVI, Hôpital Pitié-Salpétrière, Paris, France;
Unité Mixte de Recherche 146, Centre National de la Recherche Scientifique, Institut Curie, Orsay, France;
Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138;
Biomedical Research Centre, University of British Columbia, Vancouver, BC, Canada; and
¶
Theodor Kocher Institute, University of Bern, Bern, Switzerland
Based on the previous observation that RANTES mediates the cytotoxic activity of human HIV-specific CD8+ T cells via the chemokine receptor CCR3, we studied the effect of this chemokine on different effector CD8+ cytolytic cells requiring Fas/Fas ligand (FasL) or perforin-dependent pathway. In CTLs derived from PBMCs of HIV-infected patients, both the spontaneous and the RANTES-induced cytotoxicity were inhibited by anti-FasL neutralizing Abs. In contrast, allogeneic CTLs or NK cells killing through perforin were not affected by RANTES and anti-FasL Ab. Accordingly, RANTES enhanced the expression of FasL in a concentration- and time-dependent manner in HIV-specific CTLs, whereas anti-RANTES Ab decreased markedly FasL expression. Finally, cell surface expression of FasL protein in HIV-specific CTLs was also up-regulated by eotaxin, a selective ligand for CCR3. Our observations show that the action of RANTES via CCR3 is necessary to regulate FasL expression on HIV-specific CD8+ T cells that kill through the Fas/FasL pathway.
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