IL-13Ra1-mediated signaling regulates ABC expansion and lupus pathogenesis

ABCs are an emerging B cell subset that aberrantly expand in SLE. ABC generation and differentiation exhibit marked sexual dimorphism and TLR7 engagement is a key contributor to these sex differences. ABC generation is also controlled by IL-21 and its interplay with IFNg and IL-4. Here we investigated whether IL-13Ra1, an X-linked receptor that transmits IL-4/IL-13 signals, can regulate ABCs and lupus pathogenesis. 7 samples: 4 DKO, 3 IL13KO+DKO contributor: HSS Genomics Research CenterABC细胞（ABCs）是一类新兴的B细胞亚群，可在系统性红斑狼疮（SLE, Systemic Lupus Erythematosus）中发生异常扩增。ABC细胞的产生与分化过程呈现显著的性别二态性，而Toll样受体7（TLR7, Toll-like Receptor 7）的激活是造成此类性别差异的关键诱因。ABC细胞的产生同时受白细胞介素21（IL-21, Interleukin-21）调控，并与其与干扰素γ（IFNg, Interferon γ）、白细胞介素4（IL-4, Interleukin-4）的相互作用密切相关。本研究旨在探究可传递IL-4/IL-13信号的X连锁受体IL-13受体α1（IL-13Ra1, Interleukin-13 Receptor Alpha 1）是否能够调控ABC细胞的生物学行为以及狼疮的发病机制。本研究共纳入7份实验样本：4份为双基因敲除（DKO, Double Knockout）样本，3份为IL13敲除+双基因敲除（IL13KO+DKO）样本。本研究的贡献方为HSS基因组研究中心（HSS Genomics Research Center）。