Association of the HLA-G 14 bp polymorphism with systemic lupus erythematosus

• Published in: Lupus Vol. 18; no. 5; pp. 424 - 430
• Main Authors: Veit, TD, Cordero, EAA, Mucenic, T, Monticielo, OA, Brenol, JCT, Xavier, RM, Delgado-Cañedo, A, Chies, JAB
• Format: Journal Article
• Language: English
• Published: London, England SAGE Publications 01-04-2009; Sage Publications Ltd
• Subjects: Adolescent; Adult; African Continental Ancestry Group - genetics; Antigens; Arthritis; Case-Control Studies; European Continental Ancestry Group - genetics; Female; Gene Deletion; Gene Frequency - genetics; Genetic Predisposition to Disease - genetics; Heterozygote; Histocompatibility Antigens Class I - genetics; HLA Antigens - genetics; HLA-G Antigens; Hospitals; Humans; Immunology; Inflammatory diseases; Leukocytes; Lupus; Lupus Erythematosus, Systemic - genetics; Male; Patients; Photosensitivity Disorders - genetics; Polymerase chain reaction; Polymorphism; Polymorphism, Single Nucleotide - genetics; Rheumatology; Skin; Young Adult; Brazil; HLA-G; systemic lupus erythematosus; polymorphism
• ISSN: 0961-2033; 1477-0962
• DOI: 10.1177/0961203308098187

Human leukocyte antigen-G (HLA-G) is a nonclassical class I major histocompatibility complex molecule which is induced at the course of inflammatory pathologies, and its expression has been suggested as a possible mechanism of tissue protection against autoimmune inflammatory responses, therefore acting as a mechanism of immune surveillance. We investigated the influence of the 14 bp polymorphism of the HLA-G gene on systemic lupus erythematosus (SLE) by analyzing 293 patients with SLE and 460 healthy controls. The patient’s group was not in Hardy–Weinberg equilibrium, presenting an excess of heterozygotes (P = 0.014). The heterozygote group exhibited lower systemic lupus erythematosus disease activity indexes than the homozygous deletion group and the homozygous insertion group (mean value = 2.29 against 2.97 and 3.4, respectively, P = 0.035). Photosensitive patients showed a higher frequency of heterozygotes and an equivalent lower frequency of homozygotes for deletion; on the other hand, patients without arthritis presented a higher frequency of heterozygotes than the arthritis group and also a lower frequency of the del/del genotype. Overall, our results support the idea of a role of the HLA-G insertion/deletion polymorphism and therefore a role for the HLA-G molecule, on the pathology of SLE.