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* Centre d’Immunologie de Marseille-Luminy, Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de la Méditerranée, Campus de Luminy, Marseille, France;
Department of Molecular Microbiology and Immunology, Brown University, Providence, RI 02912;
Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037;
Unité de Biologie Moléculaire du Gène, INSERM Unité 277, Institut Pasteur, Paris, France;
¶ Gastroenterology Division, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115;
|| Abramson Family Cancer Research Institute and Department of Medicine, University of Pennsylvania, Philadelphia, PA 19104;
# Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520;
** Laboratoire d’Immunologie, INSERM Unité 520, Institut Curie, Paris, France; and
Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720
MHC class I-specific Ly49 inhibitory receptors regulate NK cell activation, thereby preventing autologous damage to normal cells. Ly49 receptors are also expressed on a subset of CD8+ T cells whose origin and function remain unknown. We report here that, despite their phenotypic and cytolytic similarities, Ly49+CD8+ T cells and conventional Ly49–CD44high memory-phenotype CD8+ T cells present strikingly distinct features. First, under steady state conditions Ly49+CD8+ T cells are poor cytokine producers (TNF-
and IFN-
) upon TCR triggering. Second, Ly49+CD8+ T cells are not induced upon various settings of Ag immunization or microbial challenge. However, Ly49 can be induced on a fraction of self-specific CD8+ T cells if CD4+ T cells are present. Finally, the size of the Ly49+CD8+ T cell subset is selectively reduced in the absence of STAT1. These results indicate that Ly49 expression is associated with a differentiation program of cytolytic CD8+ T cells triggered upon chronic antigenic exposure. They further suggest that the size of the Ly49+CD8+ T cell subset marks a history of CD8+ T cell activation that might preferentially result from endogenous inducers of inflammation rather than from microbial infections.
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