1. Rheumatoid arthritis is associated with IgG antibodies to human endogenous retrovirus gag matrix: a potential pathogenic mechanism of disease?
- Author
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Nelson PN, Roden D, Nevill A, Freimanis GL, Trela M, Ejtehadi HD, Bowman S, Axford J, Veitch AM, Tugnet N, and Rylance PB
- Subjects
- Adult, Aged, Aged, 80 and over, Arthritis, Rheumatoid blood, Enzyme-Linked Immunosorbent Assay, Female, Humans, Immunoglobulin G blood, Male, Middle Aged, Young Adult, Arthritis, Rheumatoid immunology, Gene Products, gag immunology, Immunoglobulin G immunology
- Abstract
Objective: Human endogenous retrovirus (HERV)-K10 has been implicated in the etiology and pathogenesis of rheumatoid arthritis (RA). A secondary immune response to this virus might suggest an antigen-driven response in patients. The Gag region of HERV-K10 could provide a key epitope important for immunological reactivity. We investigated the presence of IgG antibodies to this region and assessed its significance in RA., Methods: We determined an antigenic peptide on the matrix segment of HERV-K10 and developed an ELISA system to detect IgG antibodies in patients with RA and controls. The presence of antibodies to the matrix peptide (denoted as MAG1: RIGKELKQAGRKGNI) was correlated with patient details., Results: On screening patients' serum, we found a significantly higher mean IgG antibody response to MAG1 in 30 patients with RA as compared to 23 patients with inflammatory bowel disease (p = 0.003), 29 patients with osteoarthritis (p = 0.001), and 43 healthy individuals (p = 0.002). Reactivity was not observed to a control peptide possessing a nonhomologous amino acid sequence. On evaluating clinical details with serological activity, no correlation with disease duration (p = 0.128), sex (p = 0.768), or rheumatoid factor status (p = 0.576) was found., Conclusion: A significantly elevated IgG antibody response to an HERV-K10 Gag matrix peptide was observed in patients with RA, suggesting that the exposure of HERV-K10 may cause a secondary, antigenic driven immune response in RA.
- Published
- 2014
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