Journal
IMMUNITY
Volume 50, Issue 3, Pages 707-+Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2019.02.002
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Funding
- National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) [K08DK101604]
- National Heart, Lung, and Blood Institute (NLHBI) [R56HL142701]
- Larry L. Hillblom Foundation
- Sandler Asthma Basic Research Center
- UCSF Department of Laboratory Medicine
- UCSF Program for Breakthrough Biomedical Research
- American Cancer Society [PF-15-157-01-CSM]
- Swedish Society for Medical Research
- UCSF Bold & Basic fellowship
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Type 2 lymphocytes promote both physiologic tissue remodeling and allergic pathology, yet their physical tissue niches are poorly described. Here, we used quantitative imaging to define the tissue niches of group 2 innate lymphoid cells (ILC2s), which are critical instigators of type 2 immunity. We identified a dominant adventitial niche around lung bronchi and larger vessels in multiple tissues, where ILC2s localized with subsets of dendritic and regulatory T cells. However, ILC2s were most intimately associated with adventitial stromal cells (ASCs), a mesenchymal fibroblast-like subset that expresses interleukin-33 (IL-33) and thymic stromal lymphopoietin (TSLP). In vitro, ASCs produced TSLP that supported ILC2 accumulation and activation. ILC2s and IL-13 drove reciprocal ASC expansion and IL-33 expression. During helminth infection, ASC depletion impaired lung ILC2 and Th2 cell accumulation and function, which are in part dependent on ASC-derived IL-33. These data indicate that adventitial niches are conserved sites where ASCs regulate type 2 lymphocyte expansion and function.
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