title: Lack of association between HLA-G 14-bp polymorphism and systemic lupus erythematosus in a Han Chinese population.
abstract: HLA-G is a non-classical HLA-class Ib molecule with multiple immunoregulatory properties. A 14-bp insertion/deletion polymorphism in the HLA-G gene has been suggested to influence the expression of HLA-G and to associate with certain pathological conditions, including autoimmune diseases. We investigated the influence of the 14-bp insertion/deletion polymorphism in the HLA-G gene on disease susceptibility in systemic lupus erythematosus by genotyping this polymorphism in 231 patients with systemic lupus erythematosus and 367 healthy controls and analyzing the levels of soluble HLA-G in a subset of patients with systemic lupus erythematosus and healthy subjects from a Han Chinese population. No statistically significant differences were observed in the frequencies of the 14-bp insertion/deletion HLA-G alleles or genotypes between controls and patients with systemic lupus erythematosus. However, a significant increased expression of soluble HLA-G was noted in patients with systemic lupus erythematosus (mean value = 230.2 U/ml vs 118.3 U/ml in controls, p = 0.0001). Moreover, patients with high levels of soluble HLA-G presented with higher disease activity and had more neurological involvement. Our results do not support the HLA-G 14-bp insertion/deletion polymorphism as a genetic factor influencing systemic lupus erythematosus susceptibility. It is possible that the expression of soluble HLA-G in systemic lupus erythematosus is enhanced as part of a mechanism to try to restore the tolerance process towards auto-antigens and to counteract inflammation. However, the participation of this molecule in the pathological process of the disease also could not be excluded.
authors.affiliation: Institute of Rheumatology and Immunology, Affiliated Hospital, North Sichuan Medical College, PR China.
authors.forename: F-X
authors.initials: FX
authors.lastname: Wu
authors.forename: L-J
authors.initials: LJ
authors.lastname: Wu
authors.forename: X-Y
authors.initials: XY
authors.lastname: Luo
authors.forename: Z
authors.initials: Z
authors.lastname: Tang
authors.forename: M-H
authors.initials: MH
authors.lastname: Yang
authors.forename: C-M
authors.initials: CM
authors.lastname: Xie
authors.forename: N-T
authors.initials: NT
authors.lastname: Liu
authors.forename: J-G
authors.initials: JG
authors.lastname: Zhou
authors.forename: J-L
authors.initials: JL
authors.lastname: Guan
authors.forename: G-H
authors.initials: GH
authors.lastname: Yuan
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D044466:Asian People / Q000235:genetics* / Q000706:statistics & numerical data*; D002681:China / Q000453:epidemiology; D015897:Comorbidity; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D020022:Genetic Predisposition to Disease / Q000208:ethnology; D005838:Genotype; D006680:HLA Antigens / Q000097:blood / Q000235:genetics*; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I / Q000097:blood / Q000235:genetics*; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000208:ethnology* / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D055815:Young Adult
chemical_list: D006680:HLA Antigens; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I