目的以Ⅱ型胶原蛋白诱导的VSIG4-/-(C57BL-6背景)小鼠关节炎模型为研究对象,探讨VSIG4在RA疾病进程中的作用。方法取SPF级DBA/1、VSIG4-/-(C57BL-6背景)以及Ncf1-/-(C57BL-6背景)小鼠,以牛Ⅱ型胶原蛋白(CⅡ)与完全佛氏佐剂完全乳化,尾根部皮下注射,在第21天以牛Ⅱ型胶原蛋白与不完全弗氏佐剂加强免疫获得CIA模型。定期观察小鼠关节改变,并进行关节评分。用H&E染色法观察小鼠关节组织病理学改变并采用流式细胞术检测脾淋巴细胞以及腹腔巨噬细胞中TNF-α的变化。结果与Ncf1-/-及DBA/1小鼠相似,VSIG4-/-小鼠在牛Ⅱ型胶原蛋白免疫后开始出现明显的多关节肿胀,即小鼠踝关节病理检测显示明显的滑膜增生,炎症细胞浸润以及关节坏死。进一步研究发现来源于VSIG4-/-关节炎模型小鼠与同系正常小鼠相比,虽然脾淋CD4+T巴细胞分泌的TNF-α没有显著性差异(P>0.05),但是腹腔巨噬细胞分泌的TNF-α具有显著性差异(P<0.05)。结论牛Ⅱ型胶原蛋白可诱导VSIG4-/-小鼠的关节炎,而腹腔巨噬细胞分泌的TNF-α在其发病过程中可能起关键作用。 OBJECTIVE: To investigate the role of VSIG4 in the pathogenesis of RA in the arthritis model induced by type II collagen in VSIG4 - / - (C57BL-6 background) mice. Methods Mice of SPF grade DBA / 1, VSIG4 - / - (C57BL-6 background) and Ncf1 - / - (C57BL-6 background) were completely emulsified with complete collagen Ⅱ (C Ⅱ) The rats were injected subcutaneously at the base of the tail and CIA models were immunized on day 21 with bovine type II collagen and incomplete Freund’s adjuvant. The mice were regularly observed joint changes, and joint score. H & E staining was used to observe the pathological changes of the joints in mice. The changes of TNF-α in splenic lymphocytes and peritoneal macrophages were detected by flow cytometry. Results Similar to Ncf1 - / - and DBA / 1 mice, VSIG4 - / - mice started to show obvious multi - joint swelling after the bovine type Ⅱ collagen immunization. The pathological examination of the mouse ankle showed obvious synovial hyperplasia, Inflammatory cell infiltration and joint necrosis. Further study found that, compared with normal mice, VSIG4 - / - arthritis model mice showed no significant difference in TNF-α secreted by splenic CD4 + T cells (P> 0.05). However, peritoneal macrophages There was a significant difference in secreted TNF-α (P <0.05). Conclusion Bovine type Ⅱ collagen can induce arthritis in VSIG4 - / - mice, whereas TNF-α secreted by peritoneal macrophages may play a key role in the pathogenesis of VSIG4 - / - mice.