Complement Regulatory Protein MCP; CD46 in Rheumatoid Arthritis

Abstract

Event Abstract Back to Event Complement Regulatory Protein MCP; CD46 in Rheumatoid Arthritis Roma Pahwa1, Uma Kumar2 and Nibhriti Das1* 1 All India Institute of Medical Sciences, Biochemistry, India 2 All India Institute of Medical Sciences, Deptt. of Medicine, India Introduction: Rheumatoid Arthritis (RA) is a chronic inflammatory disease characterized by pain, swelling and progressive destruction of multiple joints, affecting approximately 1% of the adult human population. The growing importance of Membrane cofactor protein (MCP; CD46) not only as central membrane bound complement inhibitor but also as critical regulator of T-cell immunity, suggests that regulation of its expression may have significant effects on health and disease. Objectives: Studies on animal models suggest disease modulating activity of Leukocyte CD 46 (L-CD46) in autoimmune disorders. We conducted a case-control study to explore the role of L-CD 46 in human RA. Methodology: The L-CD46 expression in 40 healthy controls and 40 RA patients on different leukocyte subpopulations was observed by Flow cytometry and expression at mRNA level was monitored using Real-Time PCR. The clinical parameters Circulating Immune Complexes (CIC), Disease activity scores (DAS28), swollen and tender joint counts (SJC and TJC) were determined and correlated with L-CD46 expression in patients. Results: In patients, the L-CD 46 expression reduced significantly on lymphocytes followed by monocytes. Further L-CD 46 transcripts declined significantly in patients. Significant inverse correlations of L-CD 46 expression on lymphocyte and monocyte surface and transcript level with DAS28, SJC and CIC were observed in patients. Conclusions: Decline in the L-CD 46 levels suggests failure in protective role of L-CD 46 against complement mediated damage in RA patients. The negative correlations of L-CD 46 with disease activity indices suggest its significant association with the disease state. Follow-up study confirming L-CD 46 role as pivotal biomarker is warranted. Keywords: Rheumatoid arthritis, MCP, CD46, complement, Inflammation Conference: 15th International Congress of Immunology (ICI), Milan, Italy, 22 Aug - 27 Aug, 2013. Presentation Type: Abstract Topic: Immune-mediated disease pathogenesis Citation: Pahwa R, Kumar U and Das N (2013). Complement Regulatory Protein MCP; CD46 in Rheumatoid Arthritis. Front. Immunol. Conference Abstract: 15th International Congress of Immunology (ICI). doi: 10.3389/conf.fimmu.2013.02.00423 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 09 Apr 2013; Published Online: 22 Aug 2013. * Correspondence: Dr. Nibhriti Das, All India Institute of Medical Sciences, Biochemistry, New Delhi, India, nibhriti@gmail.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Roma Pahwa Uma Kumar Nibhriti Das Google Roma Pahwa Uma Kumar Nibhriti Das Google Scholar Roma Pahwa Uma Kumar Nibhriti Das PubMed Roma Pahwa Uma Kumar Nibhriti Das Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.