Fc receptor beta chain deficiency exacerbates murine arthritis in the anti-type II collagen antibody-induced experimental model.
Fc receptor beta chain deficiency exacerbates murine arthritis in the anti-type II collagen antibody-induced experimental model.
复制标题
在抗 II 型胶原抗体诱导的实验模型中，Fc 受体 β 链缺陷会加剧小鼠关节炎。
DOI：
10.1007/s10165-012-0749-z
复制
发表时间：
2013
期刊：
影响因子：
--
通讯作者：
Ra C.
中科院分区：
文献类型：
--
作者：
Ohtsubo-Yoshioka M;Nunomura S;Kataoka TR;Okayama Y;Ra C.
目的Fc受体β链(FcRβ)在肥大细胞(MC)或嗜碱性粒细胞等免疫细胞中是FcγRIII的信号成分。最近的研究报道，FcγRIII参与了关节炎炎症的发展。这些发现提示FcR-β在关节炎的发病机制中可能起着关键作用。为了解决这种可能性，我们用小鼠模型研究了FcRβ在关节炎中的作用。方法为了诱导关节炎，我们给C57BL/6J小鼠(Fcrβ+/+)和Fcrβ−/−小鼠静脉注射了2 mg抗II型胶原(CII)单抗(MAbs)。3天后，腹腔注射100g脂多糖(μ；Escherichia coli055：B5)。通过检查评价关节肿胀程度。结果在脂多糖和抗CII单抗诱导的实验性关节炎模型中，Fcrβ−/−小鼠表现出关节炎症加重，表现为足爪肿胀、白细胞渗入膝关节、骨侵蚀和组织细胞因子的表达。结论Fcrβ对实验性关节炎模型中的关节炎炎症有明显的负性调节作用。
ObjectiveFc receptor β chain (FcRβ) acts as a signaling component of FcγRIII in immune cells such as mast cells (MCs) or basophils. Recent studies reported that FcγRIII contributes to the development of arthritic inflammation. These findings suggest that FcRβ may play a pivotal role in the pathogenesis of arthritic inflammation. To address this possibility, we examined the function of FcRβ in arthritic inflammation employing a mouse model.MethodsFor the induction of arthritis, we injected 2 mg of a cocktail of anti-type II collagen (CII) monoclonal antibodies (mAbs) into C57BL/6J mice (FcRβ+/+) and FcRβ−/−mice intravenously. Three days later, 100 μg lipopolysaccharide (LPS;Escherichia coli055:B5) was intraperitoneally injected. Joint swelling was evaluated by inspection. Histopathology of joint tissues was examined by hematoxylin and eosin (H&E) or tartrate-resistant acid phosphatase staining.ResultsHere, we demonstrate in a well-established experimental arthritis model induced by LPS and anti-CII mAbs that FcRβ−/−mice exhibit exacerbated arthritic inflammation manifested in paw swelling, leukocyte infiltration into the knee joint, and bone erosion and tissue cytokine expression.ConclusionOur findings clearly indicate that FcRβ negatively regulates arthritic inflammation in an experimental arthritis model.