The role of FcγR signaling in the K/B x N serum transfer model of arthritis
The role of FcγR signaling in the K/B x N serum transfer model of arthritis
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DOI：
10.4049/jimmunol.169.11.6604
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发表时间：
2002-12-01
影响因子：
4.4
通讯作者：
Crain, B
中科院分区：
文献类型：
--
作者：
Corr, M;Crain, B
KRN转基因小鼠（K/BxN）模型中的自发性关节炎是由于转基因TCR的自身反应性和随后诱导的针对葡萄糖-6-磷酸异构酶的自身抗体所致。这些自身抗体将临床上明显的关节炎转移到大多数受体小鼠品系中，并且所转移的Ab的全身性catalysis减弱爪肿胀。尽管FcgammaR共同γ链缺陷的小鼠在接受K/BxN血清后未显示临床滑膜炎，但骨中的侵蚀性病变仍发生。进一步的分析表明，Fc γ RII（-/-）小鼠表现出加速的关节炎，而Fc γ RIII（-/-）小鼠具有更缓慢进展的关节炎。爪肿胀需要骨髓来源的细胞和肥大细胞的Fc γ R表达实质上有助于爪肿胀的急性期。在关节炎的K/BxN血清转移模型中，存在临床上明显的急性期，其由Fc γ RII和Fc γ RIII调节，以及亚急性组分，其导致骨侵蚀，即使在不存在Fc γ R信号传导的情况下。
Spontaneous arthritis in the KRN transgenic mouse (K/BxN) model is due to the autoreactivity of the transgenic TCR and subsequent induction of autoantibodies directed against glucose-6-phosphate isomerase. These autoantibodies transfer clinically apparent arthritis into most recipient mouse strains and systemic catabolism of the transferred Abs attenuates paw swelling. Although mice deficient in the common gamma-chain of the FcgammaR did not show clinical synovitis after receiving K/BxN sera, erosive lesions in the bone still developed. Further analysis demonstrated that FcgammaRII(-/-) mice manifested accelerated arthritis whereas the FcgammaRIII(-/-) mice had a more slowly progressing arthritis. Paw swelling required FcgammaR expression by bone marrow-derived cells and mast cells substantially contributed to the acute phase of paw swelling. In the K/BxN serum transfer model of arthritis, there is a clinically apparent acute phase, which is modulated by FcgammaRII and FcgammaRIII, and a subacute component, which results in bone erosion, even in the absence of FcgammaR signaling.