Regulation of HLA class I surface expression requires CD99 and p230/golgin-245 interaction
| Autor: | Paul A. Gleeson, Aurore Brémond, Alain Bernard, Ophélie Meynet, Karim Mahiddine, Katia Scotlandi, Mélanie Tichet, Sylvie Coito, Ghislaine Bernard, Pierre Gounon, Jean Philippe Breittmayer |
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| Rok vydání: | 2009 |
| Předmět: |
Immunology
Golgi Apparatus Human leukocyte antigen 12E7 Antigen CD8-Positive T-Lymphocytes Antiviral Agents Autoantigens Biochemistry Jurkat cells Interferon-gamma Jurkat Cells symbols.namesake Cytosol Antigen Antigens CD HLA Antigens MHC class I Humans Transport Vesicles Immunity Cellular biology Histocompatibility Antigens Class I Membrane Proteins Cell Biology Hematology Golgi apparatus Protein Structure Tertiary Up-Regulation Cell biology Transport protein Protein Transport Transmembrane domain biology.protein symbols Cell Adhesion Molecules CD8 |
| Zdroj: | Blood. 113:347-357 |
| ISSN: | 1528-0020 0006-4971 |
| DOI: | 10.1182/blood-2008-02-137745 |
| Popis: | 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-γ 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. |
| Databáze: | OpenAIRE |
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