B1a cells play a pathogenic role in the development of autoimmune arthritis.
B1a cells play a pathogenic role in the development of autoimmune arthritis.
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B1a细胞在自身免疫性关节炎的发展中发挥致病作用
DOI：
10.18632/oncotarget.8244
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发表时间：
2016-04-12
期刊：
影响因子：
--
通讯作者：
Lu L
中科院分区：
文献类型：
--
作者：
Deng J;Wang X;Chen Q;Sun X;Xiao F;Ko KH;Zhang M;Lu L
B1细胞的功能失调与各种自身免疫性疾病的疾病进展有关，但B1细胞是否参与自身免疫性关节炎的发病机制仍不清楚。在这项研究中，我们发现，腹膜B1a细胞进行增殖，并迁移到炎症关节组织与上调RANKL表达在小鼠胶原诱导关节炎（CIA）的发展。连续转移B1a细胞加剧了关节炎的严重程度和关节损伤，而腹腔内消耗B1细胞改善了CIA小鼠的关节炎症状和关节病理学。在培养物中，RANKL表达B1 a细胞显著促进了骨髓细胞来源的破骨细胞的扩增，这与B1 a细胞转移CIA小鼠中破骨细胞生成增加的体内结果雅阁。总之，这些结果证明了B1a细胞通过RANKL介导的破骨细胞生成在自身免疫性关节炎发展中的致病作用。
Dysregulated functions of B1 cells have been implicated in the disease progression of various autoimmune disorders, but it remains largely unclear whether B1 cells are involved in the pathogenesis of autoimmune arthritis. In this study, we found that peritoneal B1a cells underwent proliferation and migrated to the inflamed joint tissue with upregulated RANKL expression during collagen-induced arthritis (CIA) development in mice. Adoptive transfer of B1a cells exacerbated arthritic severity and joint damage while intraperitoneal depletion of B1 cells ameliorated both arthritic symptoms and joint pathology in CIA mice. In culture, RANKL-expressing B1a cells significantly promoted the expansion of osteoclasts derived from bone marrow cells, which were in accord with the in vivo findings of increased osteoclastogenesis in CIA mice transferred with B1a cells. Together, these results have demonstrated a pathogenic role of B1a cells in the development of autoimmune arthritis through RANKL-mediated osteoclastogenesis.