Serum concentration of immunoglobulin G‐type antibodies against the whole Epstein–Barr nuclear antigen 1 and its aa35–58 or aa398–404 fragments in the sera of patients with systemic lupus erythematosus and multiple sclerosis

• Published in: Clinical and experimental immunology Vol. 171; no. 3; pp. 255 - 262
• Main Authors: Csuka, D., Simon, D., Hóbor, R., Uray, K., Prohászka, Z., Bánlaki, Z., Jani, P. K., Szilágyi, Á., Hudecz, F., Rajczy, K., Beke, G., Boros Major, A., Tordai, A., Illés, Z., Berki, T., Czirják, L., Füst, G.
• Format: Journal Article
• Language: English
• Published: England Oxford University Press 01.03.2013; Blackwell Publishing Ltd
• Subjects: Adult; Alleles; Amino Acid Sequence; Autoimmune diseases; Case-Control Studies; Data processing; EBNA-1 protein; Environmental factors; Enzyme-linked immunosorbent assay; Epstein-Barr virus; Epstein-Barr Virus Nuclear Antigens - immunology; Female; Genotyping; Heterozygote; Histocompatibility antigen HLA; HLA; HLA-DRB1 Chains - genetics; Humans; Immunoglobulin G; Immunoglobulin G - blood; Immunoglobulin G - immunology; Immunoglobulins; Infection; Leukocytes; Lupus Erythematosus, Systemic - blood; Lupus Erythematosus, Systemic - immunology; Male; Middle Aged; Molecular Sequence Data; Multiple sclerosis; Multiple Sclerosis - blood; Multiple Sclerosis - immunology; Original; Peptide Fragments - blood; Peptide Fragments - immunology; Risk factors; Systemic lupus erythematosus
• ISSN: 0009-9104; 1365-2249
• DOI: 10.1111/cei.12022

Summary Several studies suggest that infection by Epstein–Barr virus (EBV) might be one of the environmental factors which facilitates the development of autoimmune disorders in genetically susceptible individuals. Recent data indicate that high anti‐Epstein–Barr nuclear antigen 1 (EBNA)‐1 immunoglobulin (Ig)G titre is a strong risk factor for multiple sclerosis (MS) in patients both with and without the main genetic predisposing trait, human leucocyte antigen (HLA)‐DRB1*15:01. Because no similar studies have been published in systemic lupus erythematosus (SLE) patients, we determined the HLA‐DRB1*15:01 carrier state and the serum titres against the whole EBNA‐1 and its small fragments aa35–58 and aa398–404 in 301 SLE patients, 135 MS patients and in 345 healthy controls. The carrier state of the HLA‐DRB1*15:01 allele was deduced from genotyping of a tagSNP (rs3135388) by applying a Taqman‐based assay. The serum concentrations of antibodies to EBNA‐1 and its aa35–58 or aa398–404 fragments were determined using a commercial assay (ETI‐EBNA‐G) and home‐made enzyme‐linked immunosorbent assays, respectively. The serum concentration of anti‐EBNA‐1 antibodies was significantly (P < 0·001) higher both in MS and SLE patients than in controls. Similar significant differences were found both in HLA‐DRB1*15:01 carriers and non‐carriers. Furthermore, titres of antibodies against the aa35–58 EBNA‐1 fragment were elevated both in MS and SLE patients. By contrast, the levels of aa398–404 EBNA‐1 antibodies were elevated significantly only in the SLE patients. These findings indicate that high anti‐EBNA‐1 IgG titres are HLA‐DRB1*15:01‐independent risk factors not only for MS, but also for SLE, while high antibody titres against the aa398–404 fragment are characteristic for SLE.