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 Blood, 8 January 2009, Vol. 113, No. 2, pp. 347-357.
Prepublished online as a Blood First Edition Paper on October 10, 2008; DOI 10.1182/blood-2008-02-137745.

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IMMUNOBIOLOGY

Regulation of HLA class I surface expression requires CD99 and p230/golgin-245 interaction

Aurore Brémond1,2,*, Ophélie Meynet1,2,*, Karim Mahiddine1,2, Sylvie Coito1,2, Mélanie Tichet1,2, Katia Scotlandi3, Jean-Philippe Breittmayer1,2,4, Pierre Gounon5, Paul A. Gleeson6, Alain Bernard1,2,4, and Ghislaine Bernard1,2,4

1 Inserm UMR 576, Nice, France; 2 Université Nice-Sophia, Antipolis, France; 3 Laboratorio di Ricerca Oncologica, Istituti Ortopedici Rizzoli, Bologna, Italy; 4 CHU Nice, Hôpital de l'Archet, Laboratoire d'Immunologie, Nice, France; 5 Centre Commun de Microscopie Faculté des Sciences, Parc Valrose Nice, France; and 6 Department of Biochemistry and Molecular Biology and Bio21 Molecular Science and Biotechnology Institute, University of Melbourne, Melbourne, Australia

By presenting antigenic peptides on the cell surface, human leukocyte antigen (HLA) class I molecules are critical for immune defense. Their surface density determines, to a large extent, the level of CD8+ T cell–dependent immune reactions; their loss is a major mechanism of immune escape. Therefore, powerful processes should regulate their surface expression. Here we document the mechanisms used by CD99 to mediate HLA class I modulation. Up-regulation of HLA class I by IFN-{gamma} requires CD99. In the trans Golgi network (TGN), and up to the cell surface, CD99 and HLA class I are physically associated via their transmembrane domain. CD99 also binds p230/golgin-245, a coiled-coil protein that recycles between the cytosol and buds/vesicles of the TGN and which plays a fundamental role in trafficking transport vesicles. p230/golgin-245 is anchored within TGN membranes via its Golgin-97, RanBP1, IMh1p, P230 (GRIP) domain and the overexpression of which leads to surface and intracellular down-modulation of HLA class I molecules.


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