Group 2 innate lymphoid cells support hematopoietic recovery under stress conditions

Takao Sudo, Yasutaka Motomura, Daisuke Okuzaki, Tetsuo Hasegawa, Takafumi Yokota, Junichi Kikuta, Tomoka Ao, Hiroki Mizuno, Takahiro Matsui, Daisuke Motooka, Ryosuke Yoshizawa, Takashi Nagasawa, Yuzuru Kanakura, Kazuyo Moro, Masaru Ishii

研究成果: Article査読

1 被引用数 (Scopus)

抄録

The cell-cycle status of hematopoietic stem and progenitor cells (HSPCs) becomes activated following chemotherapy-induced stress, promoting bone marrow (BM) regeneration; however, the underlying molecular mechanism remains elusive. Here we show that BM-resident group 2 innate lymphoid cells (ILC2s) support the recovery of HSPCs from 5-fluorouracil (5-FU)-induced stress by secreting granulocyte-macrophage colony-stimulating factor (GM-CSF). Mechanistically, IL-33 released from chemosensitive B cell progenitors activates MyD88-mediated secretion of GM-CSF in ILC2, suggesting the existence of a B cell-ILC2 axis for maintaining hematopoietic homeostasis. GM-CSF knockout mice treated with 5-FU showed severe loss of myeloid lineage cells, causing lethality, which was rescued by transferring BM ILC2s from wild-type mice. Further, the adoptive transfer of ILC2s to 5-FU-treated mice accelerates hematopoietic recovery, while the reduction of ILC2s results in the opposite effect. Thus, ILC2s may function by "sensing" the damaged BM spaces and subsequently support hematopoietic recovery under stress conditions.

本文言語English
論文番号e20200817
ジャーナルJournal of Experimental Medicine
218
5
DOI
出版ステータスPublished - 01-03-2021

All Science Journal Classification (ASJC) codes

  • 医学(全般)

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