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

Aurore Brémond, Ophélie Meynet, Karim Mahiddine, Sylvie Coito, Mélanie Tichet, Katia Scotlandi, Jean Philippe Breittmayer, Pierre Gounon, Paul A. Gleeson, Alain Bernard, Ghislaine Bernard

Research output: Contribution to journalArticlepeer-review


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-7 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.

Original languageEnglish
Pages (from-to)347-357
Number of pages11
Issue number2
Publication statusPublished - Jan 8 2009

ASJC Scopus subject areas

  • Hematology
  • Biochemistry
  • Cell Biology
  • Immunology


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