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MITA couples with PI3K to regulate actin reorganization during BCR activation

By Yukai Jing, Danqing Kang, Lu Yang, Panpan Jiang, Na Li, Jiali Cheng, Jingwen Li, Heather Miller, Boxu Ren, Quan Gong, Wei Yin, Zheng Liu, Pieta K. Mattila, Bing Yu, Chaohong Liu

Posted 15 Jun 2018
bioRxiv DOI: 10.1101/346445

As an adaptor protein, MITA has been extensively studied in innate immunity. However, its role in adaptive immunity as well as its underlying mechanism are not completely understood. We studied the effect of MITA deficiency on B cell development and differentiation, BCR signaling and humoral immune response. We found that MITA deficiency promotes the differentiation of marginal zone B cells, which is linked to the lupus-like autoimmune disease . MITA is involved in BCR activation and negatively regulates the activation of CD19 and Btk and positively regulates the activation of SHIP. Interestingly, we found that the activation of WASP and accumulation of F-actin is enhanced in MITA KO B cells upon stimulation. Mechanistically, we found that MITA uses PI3K mediated by the CD19-Btk axis as a central hub to control the actin remodeling that, in turn, offers feedback to BCR signaling. Overall, our study has provided a new mechanism on how MITA regulates BCR signaling via feedback from actin reorganization, which may contribute to the effects of MITA on the humoral immune response.

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