IL-33 promotes the egress of group 2 innate lymphoid cells from the bone marrow

Matthew T. Stier, Jian Zhang, Kasia Goleniewska, Jacqueline Y. Cephus, Mark Rusznak, Lan Wu, Luc Van Kaer, Baohua Zhou, Dawn C. Newcomb, R. Stokes Peebles

Research output: Contribution to journalArticle

64 Scopus citations


Group 2 innate lymphoid cells (ILC2s) are effector cells within the mucosa and key participants in type 2 immune responses in the context of allergic inflammation and infection. ILC2s develop in the bone marrow from common lymphoid progenitor cells, but little is known about how ILC2s egress from the bone marrow for hematogenous trafficking. In this study, we identified a critical role for IL-33, a hallmark peripheral ILC2-activating cytokine, in promoting the egress of ILC2 lineage cells from the bone marrow. Mice lacking IL-33 signaling had normal development of ILC2s but retained significantly more ILC2 progenitors in the bone marrow via augmented expression of CXCR4. Intravenous injection of IL-33 or pulmonary fungal allergen challenge mobilized ILC2 progenitors to exit the bone marrow. Finally, IL-33 enhanced ILC2 trafficking to the lungs in a parabiosis mouse model of tissue disruption and repopulation. Collectively, these data demonstrate that IL-33 plays a critical role in promoting ILC2 egress from the bone marrow.

Original languageEnglish (US)
Pages (from-to)263-281
Number of pages19
JournalJournal of Experimental Medicine
Issue number1
StatePublished - Jan 1 2018

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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