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Prepublished online as a Blood First Edition Paper on April 30, 2002; DOI 10.1182/blood-2001-12-0276. This Article Full Text (PDF) All Versions of this Article: 2001-12-0276v1 100/1/350    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Ronchetti, S. Articles by Pandolfi, P. P. Search for Related Content PubMed PubMed Citation Articles by Ronchetti, S. Articles by Pandolfi, P. P. Social Bookmarking                   What's this? Submitted December 18, 2001 Accepted February 24, 2002 Role of GITR in activation response of T lymphocytes Simona Ronchetti, Giuseppe Nocentini, Carlo Riccardi*, and Pier Paolo Pandolfi Department of Clinical and Experimental Medicine, Section of Pharmacology, Perugia University Medical School, Perugia, Italy; Molecular Biology Program, Department of Pathology, Memorial Sloan Kettering Cancer Center, Sloan-Kettering Division, Graduate School of Medical Sciences, Cornell University, New York, New York, USA Department of Clinical and Experimental Medicine, Section of Pharmacology, Perugia University Medical School, Perugia, Italy ; Molecular Biology Program, Department of Pathology, Memorial Sloan Kettering Cancer Center, Sloan-Kettering Division, Graduate School of Medical Sciences, Cornell University, New York, New York, USA * Corresponding author; email: riccardi{at}unipg.it. In this study, we describe the generation and characterisation of mice in which GITR gene (TNFRSF18), a member of the TNFRSF family mainly expressed on T lymphocytes, has been ablated (GITR-/- mice). Results indicate that GITR inactivation does not impair the normal development of the lymphoid organs but modulates T cell activation. In fact, when GITR-/- T lymphocytes are activated by treatment with an anti-CD3 monoclonal antibody they proliferate more than wild type cells. Moreover, activated GITR-/- T lymphocytes express higher levels of IL-2 receptor (IL-2R), produce larger amounts of IL-2 and are more sensitive to activation-induced cell death (AICD) than controls. These results suggest that GITR is involved in the regulation of TCR/CD3-driven T-cell activation and programmed cell death. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: R. W. van Olffen, N. Koning, K. P. J. M. van Gisbergen, F. M. 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