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

• Published in: Blood Vol. 113; no. 2; pp. 347 - 357
• Main Authors: Brémond, Aurore, Meynet, Ophélie, Mahiddine, Karim, Coito, Sylvie, Tichet, Mélanie, Scotlandi, Katia, Breittmayer, Jean-Philippe, Gounon, Pierre, Gleeson, Paul A., Bernard, Alain, Bernard, Ghislaine
• Format: Journal Article
• Language: English
• Published: Washington, DC Elsevier Inc 08.01.2009; Americain Society of Hematology
• Subjects: 12E7 Antigen; Antigens, CD - immunology; Antigens, CD - metabolism; Antiviral Agents - immunology; Antiviral Agents - pharmacology; Autoantigens - immunology; Autoantigens - metabolism; Biological and medical sciences; CD8-Positive T-Lymphocytes - immunology; CD8-Positive T-Lymphocytes - metabolism; Cell Adhesion Molecules - immunology; Cell Adhesion Molecules - metabolism; Cell physiology; Cytosol - immunology; Cytosol - metabolism; Fundamental and applied biological sciences. Psychology; Golgi Apparatus - immunology; Golgi Apparatus - metabolism; Histocompatibility Antigens Class I - biosynthesis; Histocompatibility Antigens Class I - immunology; HLA Antigens - biosynthesis; HLA Antigens - immunology; Humans; Immunity, Cellular - physiology; Interferon-gamma - immunology; Interferon-gamma - pharmacology; Jurkat Cells; Membrane and intracellular transports; Membrane Proteins - immunology; Membrane Proteins - metabolism; Molecular and cellular biology; Protein Structure, Tertiary - physiology; Protein Transport - drug effects; Protein Transport - immunology; Transport Vesicles - immunology; Transport Vesicles - metabolism; Up-Regulation - drug effects; Up-Regulation - immunology; Human; Antigen presentation; Membrane protein; Regulation(control); Leukocyte; Intercellular transport; Gene expression; Class I histocompatibility antigen

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...