| First Author | Sutherland TE | Year | 2018 |
| Journal | PLoS Pathog | Volume | 14 |
| Issue | 11 | Pages | e1007423 |
| PubMed ID | 30500858 | Mgi Jnum | J:313191 |
| Mgi Id | MGI:6791567 | Doi | 10.1371/journal.ppat.1007423 |
| Citation | Sutherland TE, et al. (2018) Ym1 induces RELMalpha and rescues IL-4Ralpha deficiency in lung repair during nematode infection. PLoS Pathog 14(11):e1007423 |
| abstractText | Ym1 and RELMalpha are established effector molecules closely synonymous with Th2-type inflammation and associated pathology. Here, we show that whilst largely dependent on IL-4Ralpha signaling during a type 2 response, Ym1 and RELMalpha also have IL-4Ralpha-independent expression patterns in the lung. Notably, we found that Ym1 has opposing effects on type 2 immunity during nematode infection depending on whether it is expressed at the time of innate or adaptive responses. During the lung migratory stage of Nippostrongylus brasiliensis, Ym1 promoted the subsequent reparative type 2 response but once that response was established, IL-4Ralpha-dependent Ym1 was important for limiting the magnitude of type 2 cytokine production from both CD4+ T cells and innate lymphoid cells in the lung. Importantly, our study demonstrates that delivery of Ym1 to IL-4Ralpha deficient animals drives RELMalpha production and overcomes lung repair deficits in mice deficient in type 2 immunity. Together, Ym1 and RELMalpha, exhibit time and dose-dependent interactions that determines the outcome of lung repair during nematode infection. |
