HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Fournel, S. Articles by Revillard, J.-P. Search for Related Content PubMed PubMed Citation Articles by Fournel, S. Articles by Revillard, J.-P.

A Noncomitogenic CD2R Monoclonal Antibody Induces Apoptosis of Activated T Cells by a CD95/CD95-L-Dependent Pathway⁴

^* Laboratory of Immunology, Institut National de la Santé et de la Recherche Médicale Unit 80 Claude Bernard University, Hôpital E. Herriot, Lyon, France; Sir William Dunn School of Pathology, Oxford University, Oxford, U.K.; and Centre National de la Recherche Scientifique URA625 Hôpital Pitié-Salpétrière, Paris, France ^§ Laboratory of Immunology, Institut National de la Santé et de la Recherche Médicale Unit 80 UCBL, Hôpital E. Herriot, Lyon, France; ^¶ Sir William Dunn School of Pathology, Oxford University, Oxford, U.K.; and ^|| Centre National de la Recherche Scientifique URA625 Hôpital Pitié-Salpétrière Paris, France

Clonal expansion of activated T and B cells is controlled by homeostatic mechanisms resulting in apoptosis of a large proportion of activated cells, mostly through interaction between CD95 (Fas or Apo-1) receptor and its ligand CD95-L. CD2, which is considered as a CD3/TCR alternative pathway of T cell activation, may trigger activation-induced cell death, but the role of CD95/CD95-L interaction in CD2-mediated apoptosis remains controversial. We show here that the CD2R mAb YTH 655.5, which does not induce comitogenic signals when associated with another CD2 mAb, triggers CD95-L expression by preactivated but not resting T cells, resulting in CD95/CD95-L-mediated apoptosis. The critical role of CD95/CD95-L interaction was supported by complete inhibition in the presence of the antagonist CD95 mAb ZB4 and by blocking CD95-L synthesis and surface expression by cycloheximide, cyclosporin A, EGTA, or cytochalasin B. YTH 655.5 was shown to stimulate p56^lck phosphorylation and enzymatic activity. However, p56^lck activation is not sufficient to trigger apoptosis, because other CD2R and CD4 mAbs that activate p56^lck do not induce apoptosis. In conclusion, CD2 can mediate nonmitogenic signals, resulting in CD95-L expression and apoptosis of CD95⁺ cells.

This article has been cited by other articles:

				S. Fournel, M. Aguerre-Girr, X. Huc, F. Lenfant, A. Alam, A. Toubert, A. Bensussan, and P. Le Bouteiller Cutting Edge: Soluble HLA-G1 Triggers CD95/CD95 Ligand-Mediated Apoptosis in Activated CD8+ Cells by Interacting with CD8 J. Immunol., June 15, 2000; 164(12): 6100 - 6104. [Abstract] [Full Text] [PDF]

				M. Mori, Y. Terui, M. Ikeda, H. Tomizuka, M. Uwai, T. Kasahara, N. Kubota, T. Itoh, Y. Mishima, M. Douzono-Tanaka, et al. beta 2-Microglobulin Identified as an Apoptosis-Inducing Factor and Its Characterization Blood, October 15, 1999; 94(8): 2744 - 2753. [Abstract] [Full Text] [PDF]