title: HLA-G and inflammatory diseases.
abstract: HLA-G antigens are non classical HLA-class I molecules characterized by a low allelic polymorphism, a limited tissue distribution and the presence of membrane bound and soluble isoforms. The HLA-G antigens were firstly detected in cytotrophoblast cells at the feto-maternal interface where they maintain a tolerogenic status between the mother and the semiallogenic fetus. Recently a variable expression of HLA-G molecules has been documented in several autoimmune diseases, viral infections, cancer diseases and transplantation. Overall the presence of HLA-G molecules in both membranes bound and soluble isoforms was associated with tolerogenic functions against innate and adaptative cellular responses. HLA-G antigens are able to affect the cytotoxicity of natural killer and CD8+ T cells, CD4+ T lymphocyte functions and dendritic cell maturation. In addition to the allelic polymorphism the HLA-G gene shows a deletion/insertion polymorphism of a 14 base pairs sequence (14bp) in the exon 8 at the 3' untranslated region. Several reports have associated the presence of the 14bp insertion allele (+14bp) to an unstable mRNA and a lower sHLA-G protein production, suggesting a different ability to counteract inflammation between genotypes. We reviewed the literature on the expression of HLA-G antigens in autoimmune and allergic diseases and the possible functional role of these molecules in counteracting inflammation.
authors.affiliation: Laboratory of Immunogenetics, Section of Medical Genetics, Department of Experimental and Diagnostic Medicine, University of Ferrara, Via Luigi Borsari 46, Ferrara, Italy. bri@unife.it
authors.forename: Olavio R
authors.initials: OR
authors.lastname: Baricordi
authors.forename: Marina
authors.initials: M
authors.lastname: Stignani
authors.forename: Loredana
authors.initials: L
authors.lastname: Melchiorri
authors.forename: Roberta
authors.initials: R
authors.lastname: Rizzo
mesh_terms: D000483:Alleles; D001172:Arthritis, Rheumatoid / Q000276:immunology / Q000378:metabolism; D001249:Asthma / Q000276:immunology / Q000378:metabolism; D002490:Central Nervous System / Q000276:immunology / Q000378:metabolism; D005091:Exons; D005767:Gastrointestinal Diseases / Q000276:immunology / Q000378:metabolism; D006680:HLA Antigens / Q000097:blood / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I / Q000097:blood / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D006801:Humans; D007108:Immune Tolerance / Q000276:immunology*; D007249:Inflammation / Q000276:immunology* / Q000378:metabolism; D016131:Lymphocyte Subsets / Q000276:immunology* / Q000378:metabolism; D020033:Protein Isoforms / Q000276:immunology / Q000378:metabolism; D012333:RNA, Messenger / Q000276:immunology / Q000378:metabolism; D012867:Skin / Q000276:immunology / Q000378:metabolism; D014327:Trophoblasts / Q000276:immunology* / Q000378:metabolism
chemical_list: D006680:HLA Antigens; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I; D020033:Protein Isoforms; D012333:RNA, Messenger