gms | German Medical Science

47. Kongress der Deutschen Gesellschaft für Rheumatologie (DGRh), 33. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie (DGORh), 29. Jahrestagung der Gesellschaft für Kinder- und Jugendrheumatologie (GKJR)

04.09. - 07.09.2019, Dresden

Differential pattern of autoantibodies targeting G protein-coupled receptors in systemic lupus erythematosus

Meeting Abstract

  • Jiao Luo - Klinik für Rheumatologie und klinische Immunologie, Universität zu Lübeck, Lübeck
  • Xiaoyang Yue - German Center for Lung Research (DZL), Borstel
  • Harald Heidecke - CellTrend GmbH, Luckenwalde
  • Antje Müller - Klinik für Rheumatologie und klinische Immunologie, Universität zu Lübeck, Lübeck
  • Xinhua Yu - German Center for Lung Research (DZL), Borstel
  • Gabriela Riemekasten - Universität zu Lübeck, Klinik für Rheumatologie und Klinische Immunologie, Lübeck

Deutsche Gesellschaft für Rheumatologie. Deutsche Gesellschaft für Orthopädische Rheumatologie. Gesellschaft für Kinder- und Jugendrheumatologie. 47. Kongress der Deutschen Gesellschaft für Rheumatologie (DGRh), 33. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie (DGORh), 29. Jahrestagung der Gesellschaft für Kinder- und Jugendrheumatologie (GKJR). Dresden, 04.-07.09.2019. Düsseldorf: German Medical Science GMS Publishing House; 2019. DocET.22

doi: 10.3205/19dgrh143, urn:nbn:de:0183-19dgrh1438

Published: October 8, 2019

© 2019 Luo et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.


Outline

Text

Background: G-protein coupled receptors are the largest super family of integral membrane proteins in human. Systemic lupus erythematosus (SLE) is multisystem autoimmune disease characterized by chronic immune activation and the presence of a plethora of autoantibodies. Our hypothesis is that autoantibodies targeting G protein-coupled receptors may have role in the pathogenesis of SLE.

Methods: Sera were obtained from patients with SLE (n=24) and age- and sex-matched healthy controls (n=52). SLE was diagnosed according to the American College of Rheumatology criteria. SLE disease activity was determined by SLEDAI-2K score. Circulating anti-β1/β2 adrenoceptor antibodies, anti-endothelin receptor A (ETAR) antibodies, anti-muscarinic acetylcholine receptor M3 antibodies, anti-C5aR antibodies, anti-CXC chemokine receptor 3 (CXCR3) antibodies and anti-CXC chemokine 4 (CXCR4) antibodies were measured by ELISA.

Results: The concentrations of anti-β1 adrenoceptor antibodies, anti-β2 adrenoceptor antibodies and anti-ETAR antibodies were higher in SLE patients than healthy controls (p<0.05). Further, the concentrations of anti-CXCR3 antibodies, anti-CXCR4 antibodies, anti-C5aR antibodies and anti-M3 receptor antibodies were lower in SLE patients than healthy controls (p<0.05). Anti-CXCR3 antibodies, anti-CXCR4 antibodies, anti-C5aR antibodies and anti-M3 receptor antibodies showed no correlation with SLEDAI-2K, complement 3 and complement 4. However, the concentrations of anti-β1/β2 adrenoceptor antibodies and anti-ETAR antibodies positively correlate with SLEDAI-2K. At the same time, the concentrations of anti-β1/β2 adrenoceptor antibodies and anti-ETAR antibodies negatively correlate with complement 3 and complement 4.

Conclusion: Autoantibodies targeting β1/β2 adrenoceptor and ETAR may have functional roles in the pathogenesis and progression of SLE.