期刊
IMMUNITY
卷 51, 期 4, 页码 709-+出版社
CELL PRESS
DOI: 10.1016/j.immuni.2019.09.005
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资金
- Boehringer Ingelheim Fonds PhD fellowship
- NIH [1K08HL130540, F32AI138458, R01 HL122531, R01 AI130019, R01 AI139536, 1K08AI123516]
- Howard Hughes Medical Institute
- Food Allergy Scientific Initiative
- Klarman Cell Observatory at the Broad Institute
Neuroimmune interactions have emerged as critical modulators of allergic inflammation, and type 2 innate lymphoid cells (ILC2s) are an important cell type for mediating these interactions. Here, we show that ILC2s expressed both the neuropeptide calcitonin gene-related peptide (CGRP) and its receptor. CGRP potently inhibited alarmin-driven type 2 cytokine production and proliferation by lung ILC2s both in vitro and in vivo. CGRP induced marked changes in ILC2 expression programs in vivo and in vitro, attenuating alarmin-driven proliferative and effector responses. A distinct subset of ILCs scored highly for a CGRP-specific gene signature after in vivo alarmin stimulation, suggesting CGRP regulated this response. Finally, we observed increased ILC2 proliferation and type 2 cytokine production as well as exaggerated responses to alarmins in mice lacking the CGRP receptor. Together, these data indicate that endogenous CGRP is a critical negative regulator of ILC2 responses in vivo.
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