Journal
NATURE IMMUNOLOGY
Volume 19, Issue 2, Pages 192-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41590-017-0030-x
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Funding
- Snyder Institute
- Canadian Foundation for Innovation-John R. Evans Leaders fund
- Alberta Enterprise and Advanced Education Research Capacity Program
- Canadian Institutes of Health Research [RS-342013]
- Department of Critical Care Medicine of the University of Calgary
- University of Calgary Medical Group
- Cumming School of Medicine Research Enhancement Program
- Canada Research Chair in Pulmonary Immunology, Inflammation and Host Defense
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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 beta(2) 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.
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