FLS是RA发病机制中的核心效应细胞,以分泌髓系分子CD11c和转录因子T-bet为特征 ,发现ABCs通过分泌TNFα及其介导的ERK1/2和JAK-STAT1途径诱导FLS活化。研究成果以“Age-associated B cells contribute to the pathogenesis of rheumatoid arthritis by inducing activation of fibroblast-like synoviocytes via TNF-α-mediated ERK1/2 and JAK-STAT1 pathways”为题发表在国际风湿病著名期刊《Annals of the Rheumatic Diseases》(IF= 27.973)
。发现FLS分泌IL-6和基质金属蛋白酶明显增多,