A hallmark of rheumatoid arthritis (RA) is the increased levels of autoantibodies preceding the onset and contributing to the classification of the disease. These autoantibodies, mainly anti-citrullinated protein antibody (ACPA) and rheumatoid factor, have been assumed to be pathogenic and many attempts have been made to link them to the development of bone erosion, pain and arthritis. We and others have recently discovered that most cloned ACPA protect against experimental arthritis in the mouse. In addition, we have identified suppressor B cells in healthy individuals, selected in response to collagen type II, and these cells decrease in numbers in RA. These findings provide a new angle on how to explain the development of RA and maybe also other complex autoimmune diseases preceded by an increased autoimmune response.

中文翻译：

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观点转变：自身免疫预防类风湿性关节炎

类风湿性关节炎 (RA) 的一个标志是发病前自身抗体水平升高，并有助于疾病的分类。这些自身抗体，主要是抗瓜氨酸蛋白抗体（ACPA）和类风湿因子，被认为是致病性的，并且已经进行了许多尝试将它们与骨侵蚀、疼痛和关节炎的发展联系起来。我们和其他人最近发现，大多数克隆 ACPA 可以预防小鼠实验性关节炎。此外，我们还在健康个体中发现了抑制性 B 细胞，这些细胞是针对 II 型胶原蛋白而选择的，并且这些细胞在 RA 中数量减少。这些发现为如何解释 RA 以及其他复杂的自身免疫性疾病的发展提供了一个新的角度。