Paul N Nelson1, Denise Roden2, Alan Nevill2, Graham L Freimanis2, Malgorzata Trela2, Hora Davari Ejtehadi2, Simon Bowman2, John Axford2, Andy M Veitch2, Nicola Tugnet2, Paul B Rylance2. 1. From the Immunology Research Group, Research Institute in Healthcare Sciences, University of Wolverhampton; the Royal Wolverhampton National Health Service Trust, New Cross Hospital, Wolverhampton; Birmingham City University; the Department of Rheumatology, University Hospitals Birmingham National Health Service Foundation Trust, Queen Elizabeth Hospital, Birmingham; Sir Joseph Hotung Centre for Musculoskeletal Disorders; St. George's University of London; National Health Service Trust, London, United Kingdom.P.N. Nelson, BSc, PhD, DipTLHE; D. Roden, BSc, MSc; A. Nevill, BSc, PhD; G.L. Freimanis, BSc, MSc, PhD; M. Trela, BSc, MSc; H.D. Ejtehadi, BSc, PhD, PGCert, DipHE, Immunology Research Group, Research Institute in Healthcare Sciences, University of Wolverhampton, Birmingham City University; S. Bowman, PhD, FRCP; N. Tugnet, BmedSci, MBCHB, PG CertMedEd, MRCP, Department of Rheumatology, University Hospitals Birmingham National Health Service Foundation Trust, Queen Elizabeth Hospital; J. Axford, DSc, MD, FRCP, FRCPCH, Sir Joseph Hotung Centre for Musculoskeletal Disorders, St. George's University of London, National Health Service Trust; A.M. Veitch, BSc, MBBS, MD, FRCP; P.B. Rylance, BSc, MBBS, CertMedEd, FRCP; The Royal Wolverhampton National Health Service Trust, New Cross Hospital. p.n.nelson@wlv.ac.uk. 2. From the Immunology Research Group, Research Institute in Healthcare Sciences, University of Wolverhampton; the Royal Wolverhampton National Health Service Trust, New Cross Hospital, Wolverhampton; Birmingham City University; the Department of Rheumatology, University Hospitals Birmingham National Health Service Foundation Trust, Queen Elizabeth Hospital, Birmingham; Sir Joseph Hotung Centre for Musculoskeletal Disorders; St. George's University of London; National Health Service Trust, London, United Kingdom.P.N. Nelson, BSc, PhD, DipTLHE; D. Roden, BSc, MSc; A. Nevill, BSc, PhD; G.L. Freimanis, BSc, MSc, PhD; M. Trela, BSc, MSc; H.D. Ejtehadi, BSc, PhD, PGCert, DipHE, Immunology Research Group, Research Institute in Healthcare Sciences, University of Wolverhampton, Birmingham City University; S. Bowman, PhD, FRCP; N. Tugnet, BmedSci, MBCHB, PG CertMedEd, MRCP, Department of Rheumatology, University Hospitals Birmingham National Health Service Foundation Trust, Queen Elizabeth Hospital; J. Axford, DSc, MD, FRCP, FRCPCH, Sir Joseph Hotung Centre for Musculoskeletal Disorders, St. George's University of London, National Health Service Trust; A.M. Veitch, BSc, MBBS, MD, FRCP; P.B. Rylance, BSc, MBBS, CertMedEd, FRCP; The Royal Wolverhampton National Health Service Trust, New Cross Hospital.
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.
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.
Authors: G Mameli; G L Erre; E Caggiu; S Mura; D Cossu; M Bo; M L Cadoni; A Piras; N Mundula; E Colombo; G Buscetta; G Passiu; L A Sechi Journal: Clin Exp Immunol Date: 2017-05-09 Impact factor: 4.330
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