The autoantigen TRIM21 as a clinical target for systemic lupus erythematosus

系统性红斑狼疮(SLE)或干燥综合征(SS)的病因仍不清楚。在这项研究中，我们研究了在SLE和SS患者血清中观察到的自身抗原TRIM21和TRIM68在这些疾病发病中的作用。我们阐明了TRIM21参与了TRAF6的泛素化，TRAF6是核因子-kappaB信号转导和促炎细胞因子产生的重要因子，并在I型干扰素表达的负性调节中发挥作用。我们还观察到TRIM68与IRF家族蛋白相互作用并泛素化它们。提示TRIM21和TRIM68在SLE和SS的发病机制中起重要作用。它们可能有潜力成为这些疾病的治疗靶点。

The etiology of systemic lupus erythematosus (SLE) or Sjogren's syndrome (SS) still remains unknown. In this study, we investigated the role of TRIM21 and TRIM68, the autoantigens observed in the sera of patients with SLE and SS, in the pathogenesis of these diseases. We clarified that TRIM21 is involved in the ubiquitylation pf TRAF6, an important factor for the NF-kappaB signaling and proinflammatory cytokine production, and that it plays a role in the negative regulation of type I interferon expression. We also observed that TRIM68 interacts with IRF family proteins and ubiquitylates them. These finding suggests that TRIM21 and TRIM68 play an important role for the pathogenesis of SLE and SS. They may have potential as a therapeutic target for these diseases.