Role of mast cell activation in the development of rheumatoid arthritis

含有IgG受体的肥大细胞参与类风湿关节炎的发病机制。IgG受体在MCs上以四聚体表达，包括Fc受体β链（Fcε riβ）。然而，FcεRIβ在类风湿关节炎发展中的作用在很大程度上是未知的。在本研究中，我们利用抗II型胶原（CII）抗体诱导的关节炎模型，研究了IgG受体信号调节因子FcεRIβ在类风湿关节炎中的作用。与WT小鼠相比，FcεRIβ-/-小鼠的关节炎严重程度增加。与这一观察结果一致，组织病理学分析显示，浸润到滑膜的淋巴细胞在FcεRIβ-/-小鼠中比在WT小鼠中更多。我们的研究结果表明，FcεRIβ在炎症反应的调节中发挥重要作用，并在关节炎的发展中发挥抑制分子的作用。

Mast cells (MCs) harboring IgG receptor contribute to the pathogenesis of rheumatoid arthritis. IgG receptor on MCs, but not on other immune cells, is expressed as a tetramer including Fc receptor β chain (FcεRIβ). However, role of FcεRIβ in the development of rheumatoid arthritis is largely unknown. In the present study we investigated the function of FcεRIβ, a regulator of IgG receptor signaling, in rheumatoid arthritis employing an anti-type II collagen (CII) Ab-induced arthritis model. FcεRIβ-/-mice exhibited increased severity of arthritis compared with WT mice. Consistent with this observation, histopathological analyses revealed that infiltrated lymphocytes into the synovium were more increased in FcεRIβ-/- mice than in WT mice. Our findings of the present study suggest that FcεRIβ plays important roles in the regulation of inflammatory responses and that it act as an inhibitory molecule in the development of arthritis.