| First Author | Inclan-Rico JM | Year | 2020 |
| Journal | Nat Immunol | Volume | 21 |
| Issue | 10 | Pages | 1181-1193 |
| PubMed ID | 32807943 | Mgi Jnum | J:305536 |
| Mgi Id | MGI:6706395 | Doi | 10.1038/s41590-020-0753-y |
| Citation | Inclan-Rico JM, et al. (2020) Basophils prime group 2 innate lymphoid cells for neuropeptide-mediated inhibition. Nat Immunol 21(10):1181-1193 |
| abstractText | Type 2 cytokine responses promote parasitic immunity and initiate tissue repair; however, they can also result in immunopathologies when not properly restricted. Although basophilia is recognized as a common feature of type 2 inflammation, the roles basophils play in regulating these responses are unknown. Here, we demonstrate that helminth-induced group 2 innate lymphoid cell (ILC2) responses are exaggerated in the absence of basophils, resulting in increased inflammation and diminished lung function. Additionally, we show that ILC2s from basophil-depleted mice express reduced amounts of the receptor for the neuropeptide neuromedin B (NMB). Critically, NMB stimulation inhibited ILC2 responses from control but not basophil-depleted mice, and basophils were sufficient to directly enhance NMB receptor expression on ILC2s. These studies suggest that basophils prime ILC2s to respond to neuron-derived signals necessary to maintain tissue integrity. Further, these data provide mechanistic insight into the functions of basophils and identify NMB as a potent inhibitor of type 2 inflammation. |
