Journal of Immunology Research
Volume 2014 (2014), Article ID 298569, 14 pages
http://dx.doi.org/10.1155/2014/298569
Review Article
1Institut National de la Santé et de la Recherche Médicale (Inserm), U.1085, Institut de Recherche sur la Santé, l'Environnement, et le Travail (IRSET), 2 Avenue du Pr. Leon Bernard CS 34317, 35043 Rennes, France
2Université de Rennes 1, 35043 Rennes, France
3Fédération de Recherche BioSit de Rennes UMS 3480, 35043 Rennes, France
4Department of Biology, University Hospital Pontchaillou, CHU Pontchaillou, 35033 Rennes, France
2Université de Rennes 1, 35043 Rennes, France
3Fédération de Recherche BioSit de Rennes UMS 3480, 35043 Rennes, France
4Department of Biology, University Hospital Pontchaillou, CHU Pontchaillou, 35033 Rennes, France
Received 8 January 2014; Revised 9 March 2014; Accepted 10 March 2014; Published 15 April 2014
Academic Editor: Roberta Rizzo
Copyright © 2014 Laurence Amiot et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
HLA-G is a nonclassical major histocompatibility complex molecule first described at the maternal-fetal interface, on extravillous cytotrophoblasts. Its expression is restricted to some tissues in normal conditions but increases strongly in pathological conditions. The expression of this molecule has been studied in detail in cancers and is now also beginning to be described in infectious diseases. The relevance of studies on HLA-G expression lies in the well known inhibitory effect of this molecule on all cell types involved in innate and adaptive immunity, favoring escape from immune control. In this review, we summarize the features of HLA-G expression by type of infections (i.e, bacterial, viral, or parasitic) detailing the state of knowledge for each pathogenic agent. The polymorphism, the interference of viral proteins with HLA-G intracellular trafficking, and various cytokines have been described to modulate HLA-G expression during infections. We also discuss the cellular source of HLA-G, according to the type of infection and the potential role of HLA-G. New therapeutic approaches based on synthetic HLA-G-derived proteins or antibodies are emerging in mouse models of cancer or transplantation, and these new therapeutic tools may eventually prove useful for the treatment of infectious diseases.
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