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Species: mouse
Number of cells: 10070
Study size: 184MB
Complement Signals Determine Opposite Effects of B Cells in Chemotherapy-Induced Immunity (Mouse)
Lu, Yiwen and Zhao, Qiyi and Liao, Jian-You and Song, Erwei and Xia, Qidong and Pan, Jiayao and Li, Yihong and Li, Jiaqian and Zhou, Boxuan and Ye, Yingying and others
Lu, Yiwen and Zhao, Qiyi and Liao, Jian-You and Song, Erwei and Xia, Qidong and Pan, Jiayao and Li, Yihong and Li, Jiaqian and Zhou, Boxuan and Ye, Yingying and others
Understanding molecular mechanisms that dictate B cell diversity is important for targeting B cells as anti-cancer treatment. Through the single-cell dissection of B cell heterogeneity in longitudinal samples of patients with breast cancer before and after neoadjuvant chemotherapy, we revealed that an ICOSL + B cell subset emerges after chemotherapy. Using three immunocompetent mouse models, we recapitulated the subset switch of human tumor-infiltrating B cells during chemotherapy. By employing B-cell-specific deletion mice, we showed that ICOSL in B cells boosts anti-tumor immunity by enhancing the effector to regulatory T cell ratio. The signature of ICOSL + B cells is imprinted by complement-CR2 signaling, which is triggered by immunogenic cell death. Moreover, we identified that CD55, a complement inhibitory protein, determines the opposite roles of B cells in chemotherapy. Collectively, we demonstrated a critical role of the B cell subset switch in chemotherapy response, which has implications in designing novel anti-cancer therapies.
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