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Ligand Binding but Undetected Functional Response of FcR after Their Capture by T Cells via Trogocytosis¹

Denis Hudrisier,^2* Béatrice Clemenceau, Stéphanie Balor, Sandrine Daubeuf,^* Eddy Magdeleine,^* Marc Daëron,^¶ Pierre Bruhns,^¶ and Henri Vié

^*Centre National de la Recherche Scientifique, Institut de Pharmacologie et de Biologie Structurale, Toulouse, France; Université de Toulouse, UPS, Institut de Pharmacologie et de Biologie Structurale, Toulouse, France; INSERM, Unité 601, Nantes, France; Institut Pasteur, Département d'Immunologie, Unité d'Allergologie Moléculaire et Cellulaire, Paris, France; and ^¶INSERM, Unité 760, Paris, France

Intercellular transfer of cell surface proteins by trogocytosis is common and could affect T cell responses. Yet, the role of trogocytosis in T cell function is still elusive, and it is unknown whether a molecule, once captured by T cells, harbors the same biological properties as in donor APC. In this study, we showed that FcR as well as the associated FcR subunit could be detected at high levels on murine and human T cells after their intercellular transfer from FcR-expressing APC. Capture of FcR occurred during coculture of T cells with FcR-expressing APC upon Ab- or Ag-mediated T cell stimulation. Once captured by T cells, FcR were expressed in a conformation compatible with physiological function and conferred upon T cells the ability to bind immune complexes and to provision B cells with this source of Ag. However, we were unable to detect downstream signal or signaling-dependent function following the stimulation of FcR captured by T cells, and biochemical studies suggested the improper integration of FcR in the recipient T cell membrane. Thus, our study demonstrates that T cells capture FcR that can efficiently exert ligand-binding activity, which, per se, could have functional consequences in T cell-B cell cooperation.

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 the Region Midi-Pyrénées and the Agence Nationale pour la Recherche.

² Address correspondence and reprint requests to Dr. Denis Hudrisier, Institut de Pharmacologie et de Biologie Structurale, Centre National de la Recherche Scientifique Unité Mixte de Recherche 5089, 205 route de Narbonne, 31077 Toulouse. E-mail address: denis.hudrisier{at}ipbs.fr

³ Abbreviations used in this paper: ADCC, Ab-dependent cell cytotoxicity; β₂m, β₂-microglobulin; BM-DC, dendritic cells generated from B6 bone marrow; DC, dendritic cell; HEL, hen egg lysozyme; IC, immune complex; mFc, murine Fc.