Chistiakov Dimitry A, Chistiakov Alexander P
Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, PA 15261, USA.
Hum Immunol. 2007 May;68(5):375-83. doi: 10.1016/j.humimm.2007.01.013. Epub 2007 Feb 15.
Autoimmunity is a multistep pathogenic process, which arises in genetically predisposing individuals as a result of the harmful influence of environmental factors causing the breakdown of immune tolerance and induction of self-reactive immune response. Recent findings resolved common pathogenic mechanisms shared between different autoimmune diseases and suggested for the existence of genetic loci that could be involved in general autoimmunity and hence contribute to susceptibility of several autoimmune diseases. To date, several loci responsible for general autoimmunity have been identified. The Fc receptor-like 3 (FCRL3) gene is one of those loci for which a significant association with a number of autoimmune diseases such as rheumatoid arthritis (RA), autoimmune thyroid disease, and systemic lupus erythematosus (SLE) has been recently shown in Japanese. However, studies in Caucasians failed to confirm a strong association of this gene with RA and SLE and therefore made questionable the putative role of FCRL3 in general autoimmunity. In this review, we discuss whether the FCRL3 gene is a newly discovered gene contributing to shared susceptibility between autoimmune diseases.
自身免疫是一个多步骤的致病过程,它在具有遗传易感性的个体中出现,是环境因素有害影响的结果,这些环境因素导致免疫耐受的破坏和自身反应性免疫反应的诱导。最近的研究结果揭示了不同自身免疫性疾病之间共有的致病机制,并提示存在可能参与一般自身免疫的基因座,从而导致几种自身免疫性疾病的易感性增加。迄今为止,已经确定了几个负责一般自身免疫的基因座。Fc受体样3(FCRL3)基因就是其中之一,最近在日本人中发现它与许多自身免疫性疾病如类风湿性关节炎(RA)、自身免疫性甲状腺疾病和系统性红斑狼疮(SLE)有显著关联。然而,在高加索人中进行的研究未能证实该基因与RA和SLE有很强的关联,因此FCRL3在一般自身免疫中的假定作用受到质疑。在这篇综述中,我们讨论FCRL3基因是否是一个新发现的、导致自身免疫性疾病之间共享易感性的基因。
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