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

Author:

Stier Matthew T.1,Zhang Jian2,Goleniewska Kasia2,Cephus Jacqueline Y.2,Rusznak Mark2,Wu Lan1,Van Kaer Luc1ORCID,Zhou Baohua3,Newcomb Dawn C.12,Peebles R. Stokes12ORCID

Affiliation:

1. Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN

2. Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN

3. Wells Center for Pediatric Research, Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN

Abstract

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.

Funder

NIH

Department of Veterans Affairs

Publisher

Rockefeller University Press

Subject

Immunology,Immunology and Allergy

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