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Helios Deficiency Has Minimal Impact on T Cell Development and Function¹

Qi Cai^*,,, Andrée Dierich^,, Mustapha Oulad-Abdelghani^,, Susan Chan^2,*,, and Philippe Kastner^2,*,,,

^* Department of Cancer Biology, Institut de Génétique et de Biologie Moléculaire et Cellulaire, INSERM Unité 964, Centre National de la Recherche Scientifique, Unité Mixte de Recherche 7104, Illkirch, France; and Faculté de Médecine, Université de Strasbourg, Strasbourg, France

Helios is a member of the Ikaros family of zinc finger transcription factors. It is expressed mainly in T cells, where it associates with Ikaros-containing complexes and has been proposed to act as a rate-limiting factor for Ikaros function. Overexpression of wild-type or dominant-negative Helios isoforms profoundly alters β T cell differentiation and activation, and endogenous Helios is expressed at strikingly high levels in regulatory T cells. Helios has also been implicated as a tumor suppressor in human T cell acute lymphoblastic leukemias. These studies suggest a central role for Helios in T cell development and homeostasis, but whether this protein is physiologically required in T cells is unclear. We report herein that inactivation of the Helios gene by homologous recombination does not impair the differentiation and effector cell function of β and T cells, NKT cells, and regulatory T cells. These results suggest that Helios is not essential for T cells, and that its function can be compensated for by other members of the Ikaros family.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by institute funds from INSERM, Centre National de la Recherche Scientifique, and Hôpital Universitaire de Strasbourg, and a grant to S.C. and P.K. from the Ligue Nationale Française Contre le Cancer (Equipe Labellisée). Q.C. was funded by a predoctoral fellowship from the Association pour le Recherche sur le Cancer.

² Address correspondence and reprint requests to Dr. Susan Chan and Dr. Philippe Kastner, Department of Cancer Biology, Institut de Génétique et de Biologie Moléculaire et Cellulaire, BP 10142, 67404 Illkirch Cedex, France. E-mail address: scpk{at}igbmc.fr

³ Abbreviations used in this paper: DC, dendritic cell; B6, C57BL/6; dn, dominant negative; HPRT, hypoxanthine phosphoribosyltransferase; Treg cell, regulatory T cell; WT, wild type.