B
Bernard Mach
Researcher at University of Geneva
Publications - 204
Citations - 17509
Bernard Mach is an academic researcher from University of Geneva. The author has contributed to research in topics: Gene & Human leukocyte antigen. The author has an hindex of 66, co-authored 203 publications receiving 16912 citations. Previous affiliations of Bernard Mach include Leibniz University of Hanover & University of Oxford.
Papers
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Journal ArticleDOI
Nomenclature for factors of the HLA system, 2010.
Steven G.E. Marsh,E. D. Albert,Walter F. Bodmer,Ronald E. Bontrop,Bo Dupont,Henry A. Erlich,Marcelo Fernandez-Vina,Daniel E. Geraghty,Rhonda Holdsworth,Carolyn Katovich Hurley,M. Lau,Keun-Seok Lee,Bernard Mach,Martin Maiers,Wolfgang R. Mayr,Carlheinz Müller,Peter Parham,Effie W. Petersdorf,Takehiko Sasazuki,Jack L. Strominger,A. Svejgaard,Paul I. Terasaki,Jean-Marie Tiercy,John Trowsdale +23 more
TL;DR: This report documents the additions and revisions to the nomenclature of HLA specificities following the principles established in previous reports.
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Complementation cloning of an MHC class II transactivator mutated in hereditary MHC class II deficiency (or bare lymphocyte syndrome)
TL;DR: The CIITA gene is essential for M HC class II gene expression and has been shown to be responsible for hereditary MHC class II deficiency.
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Regulation of MHC class II expression by interferon-gamma mediated by the transactivator gene CIITA
TL;DR: It is shown that CIITA expression is controlled and induced by IFN-gamma and is a general regulator of both inducible and constitutive MHC class II expression.
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The bare lymphocyte syndrome and the regulation of MHC expression.
Walter Reith,Bernard Mach +1 more
TL;DR: The study of RFX and CIITA has made major contributions to the comprehension of the molecular mechanisms controlling MHCII genes and has made this system into a textbook model for the regulation of gene expression.
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REGULATION OF MHC CLASS II GENES: Lessons from a Disease
TL;DR: The finding that RFX5 is a subunit of the nuclear RFX-complex has confirmed that a deficiency in the binding of this complex is indeed the molecular basis for MHC-II deficiency inThe majority of patients and made possible novel strategies designed to achieve immunomodulation via transcriptional intervention.