| First Author | Kim JH | Year | 2018 |
| Journal | Nat Immunol | Volume | 19 |
| Issue | 2 | Pages | 192-201 |
| PubMed ID | 29335647 | Mgi Jnum | J:282405 |
| Mgi Id | MGI:6380821 | Doi | 10.1038/s41590-017-0030-x |
| Citation | Kim JH, et al. (2018) Aged polymorphonuclear leukocytes cause fibrotic interstitial lung disease in the absence of regulation by B cells. Nat Immunol 19(2):192-201 |
| abstractText | Pulmonary immunity requires tight regulation, as interstitial inflammation can compromise gas exchange and lead to respiratory failure. Here we found a greater number of aged CD11b(hi)L-selectin(lo)CXCR4(+) polymorphonuclear leukocytes (PMNs) in lung vasculature than in the peripheral circulation. Using pulmonary intravital microscopy, we observed lung PMNs physically interacting with B cells via beta2 integrins; this initiated neutrophil apoptosis, which led to macrophage-mediated clearance. Genetic deletion of B cells led to the accumulation of aged PMNs in the lungs without systemic inflammation, which caused pathological fibrotic interstitial lung disease that was attenuated by the adoptive transfer of B cells or depletion of PMNs. Thus, the lungs are an intermediary niche in the PMN lifecycle wherein aged PMNs are regulated by B cells, which restrains their potential to cause pulmonary pathology. |
