Collagen-induced arthritis and related animal models: How much of their pathogenesis is auto-immune, how much is auto-inflammatory?

被引:49
作者
Billiau, Alfons [1 ]
Matthys, Patrick [1 ]
机构
[1] Univ Leuven, Rega Inst, Immunobiol Lab, B-3000 Louvain, Belgium
关键词
Arthritis; Cytokines; Adjuvant; Freund; INTERFERON-GAMMA; IFN-GAMMA; MICE LACKING; INDUCTION; RECEPTOR; SUSCEPTIBILITY; IMMUNIZATION; INHIBITION; MECHANISMS; SEVERITY;
D O I
10.1016/j.cytogfr.2011.11.003
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In this review, we discuss our studies on the pathogenesis of collagen-induced arthritis (CIA) and related mouse models for rheumatoid arthritis. Of note, these models invariably rely on the use of complete Freund's adjuvant (CFA). Our analysis has focused on explaining the dichotomous - either protective or disease-promoting - role of endogenous IFN-gamma. Induction of a myelopoietic burst by CFA was identified as an important and underestimated factor in mediating the role of IFN-gamma and other cytokines (IL-6, IL-17, GCP-2, RANK-L). Myelopoiesis provides an excess in precursors for joint-infiltrating neutrophils and osteoclasts. We postulate that classical CIA is primarily an auto-inflammatory disease, in part because of a strong innate immune response to the adjuvant. Superimposed on this, collagen-specific auto-immunity reinforces inflammatory reactivity in joints. (C) 2011 Elsevier Ltd. All rights reserved.
引用
收藏
页码:339 / 344
页数:6
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