CC chemokine receptor (CCR)-2 prevents arthritis development following infection by Mycobacterium avium.
CC chemokine receptor (CCR)-2 prevents arthritis development following infection by Mycobacterium avium.
复制标题
CC 趋化因子受体 (CCR)-2 可预防鸟分枝杆菌感染后关节炎的发展。
DOI：
10.1007/s00109-006-0039-3
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发表时间：
2006
期刊：
影响因子：
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通讯作者：
Ahuja,SeemaS
中科院分区：
文献类型：
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作者：
Quinones,MarlonP;Jimenez,Fabio;Martinez,Hernan;Estrada,CarlosA;Willmon,Opal;Dudley,Molly;Kuziel,WilliamA;Melby,PeterC;Reddick,RobertL;Ahuja,SunilK;Ahuja,SeemaS
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 withMycobacterium avium, a similar arthritis phenotype was detected inCcr2-null mice in the DBA/1j, but not in the BALB/c background. The failure to develop arthritis inCcr2-null BALB/c mice occurred in the face of high bacterial burdens and low interferon gamma (IFNγ) production. By contrast,Ccr2-null DBA/1j mice had low bacterial burdens, produced normal amounts of IFNγ, and had high titers of autoantibodies against CII. Thus, theCcr2-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 diseases. These findings also indicate thatCcr2-null DBA/1j mice might serve as a valuable model system to uncover the immunological determinants of arthritis and to test novel antiarthritic agents.
