CC chemokine receptor (CCR)-2 prevents arthritis development following infection by Mycobacterium avium

Journal of Molecular Medicine : Official Organ of the Gesellschaft Deutscher Naturforscher Und Ärzte
Marlon P QuinonesSeema S Ahuja

Abstract

The host factors that influence autoimmune arthritides such as rheumatoid arthritis have not been fully elucidated. We previously found that genetic inactivation of CC chemokine receptor 2 (CCR2) in the arthritis-prone DBA/1j mouse strain significantly increases the susceptibility of this strain to autoimmune arthritis induced by immunization with collagen type II (CII) and complete Freund's adjuvant (CFA). Here, we show that following intradermal infection with Mycobacterium avium, a similar arthritis phenotype was detected in Ccr2-null mice in the DBA/1j, but not in the BALB/c background. The failure to develop arthritis in Ccr2-null BALB/c mice occurred in the face of high bacterial burdens and low interferon gamma (IFNgamma) production. By contrast, Ccr2-null DBA/1j mice had low bacterial burdens, produced normal amounts of IFNgamma, and had high titers of autoantibodies against CII. Thus, the Ccr2-null state in an arthritic-prone genetic background leads to increased arthritis susceptibility following infectious (M. avium) and noninfectious (CII/CFA) challenges. Because CCR2 serves as a negative regulator of murine arthritis, caution might need to be exercised while testing CCR2 blockers in human arthritis or other disease...Continue Reading

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Aug 30, 2005·Annals of the New York Academy of Sciences·Nuria Godessart

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Citations

Jan 31, 2008·Clinical Reviews in Allergy & Immunology·V PordeusY Shoenfeld
Dec 29, 2009·Frontiers in Bioscience (Scholar Edition)·Zoltan SzekaneczAlisa E Koch
Mar 10, 2016·The Journal of Infectious Diseases·Carolyn A LaceyJerod A Skyberg

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