Journal
CELL
Volume 180, Issue 6, Pages 1081-+Publisher
CELL PRESS
DOI: 10.1016/j.cell.2020.02.015
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Funding
- National Key Research and Development Program of China [2017YFA0106300]
- Natural Science Foundation of China [91942309, 81672614, 81971481, 81672621, 81872155]
- Natural Science Foundation of Guangdong Province [2016A030306023, 2017A030313878, 2018A030313769]
- Pearl River S&T Nova Program of Guangzhou [201710010083, 201710010048]
- Tip-top Scientific and Technical Innovative Youth Talents of Guangdong special support program [2016TQ03R553]
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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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