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B1 cell-produced anti-phosphatidylserine antibodies contribute to lupus nephritis development via TLR-mediated Syk activation

狼疮性肾炎 系统性红斑狼疮 自身抗体 免疫学 锡克 免疫系统 抗体 磷脂酰丝氨酸 自身免疫 免疫复合物 生物 医学 信号转导 细胞生物学 内科学 酪氨酸激酶 遗传学 磷脂 疾病
作者
Liwei Lu,Kongyang Ma,Wenhan Du,Shiyun Wang,Jingyi Li,Jie Tian,Yida Xing,Xiaodan Kong,Ke Rui,Rencai Qin,Xiaoxia Zhu,Jing Wang,Cainan Luo,Haijing Wu,Fan Xiao,Lan He,hejian zou,Lijun Wu,Qianjin Lu,Dongzhou Liu
出处
期刊:Research Square - Research Square 被引量:1
标识
DOI:10.21203/rs.3.rs-2536308/v1
摘要

Abstract Autoantibodies produced by B cells play a pivotal role in the pathogenesis of systemic lupus erythematosus (SLE). However, both the cellular source of anti-phospholipid antibodies and their contributions to the development of lupus nephritis (LN) remain largely unclear. Here, we report a pathogenic role ofanti-phosphatidylserine (PS) autoantibodies in the development of LN. In cohort study and mouse models, elevated serum PS-specific IgG levels were detected in SLE patients, especially in those with nephritis, and lupus mice. The deposition of PS-specific IgG was detected in kidney biopsied of lupus nephritis patients. Both transfer of SLE PS-specific IgG and PS immunization triggered lupus-like glomerular immune complex deposition in recipient mice. ELISPOT analysis identified B1a cells as the main cell type for secreting PS-specific IgG in both lupus mice and patients. Adoptive transfer of PS-specific B1a cells accelerated PS-specific autoimmune response and renal damage in recipient lupus mice whereas depletion of B1a cells attenuated lupus progression. In culture, PS-specific B1a cells were significantly expanded upon treatment with chromatin components while blockade of TLR signal cascades by DNase I digestion, inhibitory ODN 2088 or R406 treatment profoundly abrogated chromatin-induced PS-specific IgG secretion by lupus B1a cells. Thus, our study has demonstrated that the novel anti-PS autoantibodies produced by B1 cells contribute to lupus nephritis development. Our findings that blockade of TLR/Syk signaling cascade inhibits PS-specific B1 cell expansion may provide new insight in understanding lupus pathogenesis and may help develop novel therapeutic targets for the treatment of LN in SLE.
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