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Complement Signals Determine Opposite Effects of B Cells in Chemotherapy-Induced Immunity.

Abstract：

: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. VIDEO ABSTRACT.

journal_name

Cell

journal_title

Cell

authors

Lu Y,Zhao Q,Liao JY,Song E,Xia Q,Pan J,Li Y,Li J,Zhou B,Ye Y,Di C,Yu S,Zeng Y,Su S

doi

10.1016/j.cell.2020.02.015

subject

Has Abstract

pub_date

2020-03-19 00:00:00

pages

1081-1097.e24

issue

6

eissn

0092-8674

issn

1097-4172

pii

S0092-8674(20)30159-8

journal_volume

180

pub_type

杂志文章

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