Journal
IMMUNITY
Volume 51, Issue 4, Pages 682-+Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2019.06.009
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Funding
- Intramural Research Programs of NIAMS
- NIAID
- National Institutes of Health [AI074878, AI095466, AI095608, AI102942]
- Burroughs Wellcome Fund
- Crohn's & Colitis Foundation
- Cure for IBD
- Rosanne H. Silberman Foundation
- JSPS Research Fellowship for Japanese Biomedical and Behavioral Researchers at NIH
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [ZIAAI001132] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [ZIAAR041159] Funding Source: NIH RePORTER
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Innate lymphocytes maintain tissue homeostasis at mucosal barriers, with group 2 innate lymphoid cells (ILC2s) producing type 2 cytokines and controlling helminth infection. While the molecular understanding of ILC2 responses has advanced, the complexity of microenvironmental factors impacting ILC2s is becoming increasingly apparent. Herein, we used single-cell analysis to explore the diversity of gene expression among lung lymphocytes during helminth infection. Following infection, we identified a subset of ILC2s that preferentially expressed Il5-encoding interleu kin (IL)-5, together with Ca/ca-encoding calcitonin gene-related peptide (CGRP) and its cognate receptor components. CGRP in concert with IL-33 and neuromedin U (NMU) supported IL-5 but constrained IL-13 expression and ILC2 proliferation. Without CGRP signaling, ILC2 responses and worm expulsion were enhanced. Collectively, these data point to CGRP as a context-dependent negative regulatory factor that shapes innate lymphocyte responses to alarmins and neuropeptides during type 2 innate immune responses.
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