Journal
FRONTIERS IN IMMUNOLOGY
Volume 12, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2021.645741
Keywords
particulate matter; γ δ T cell; neutrophilia; IL-17; commensal microbiome
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Funding
- National Research Foundation of Korea [NRF-2019R1F1A1059237]
- Korea Global PhD Fellowship Program (KGPF) - Korean Ministry of Science Information/Communication Technology [NRF-2016H1A2A1908163]
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The study found that commensal bacteria can promote PM-induced neutrophilia in the lung via T gamma delta 17 cells.
Particulate matter (PM) induces neutrophilic inflammation and deteriorates the prognosis of diseases such as cardiovascular diseases, cancers, and infections, including COVID-19. Here, we addressed the role of gamma delta T cells and intestinal microbiome in PM-induced acute neutrophilia. gamma delta T cells are a heterogeneous population composed of T gamma delta 1, T gamma delta 2, T gamma delta 17, and naive gamma delta T cells (T gamma delta N) and commensal bacteria promote local expansion of T gamma delta 17 cells, particularly in the lung and gut without affecting their V gamma repertoire. T gamma delta 17 cells are more tissue resident than T gamma delta 1 cells, while T gamma delta N cells are circulating cells. IL-1R expression in T gamma delta 17 cells is highest in the lung and they outnumber all the other type 17 cells such as Th17, ILC3, NKT17, and MAIT17 cells. Upon PM exposure, IL-1 beta-secreting neutrophils and IL-17-producing T gamma delta 17 cells attract each other around the airways. Accordingly, PM-induced neutrophilia was significantly relieved in gamma delta T- or IL-17-deficient and germ-free mice. Collectively, these findings show that the commensal microbiome promotes PM-induced neutrophilia in the lung via T gamma delta 17 cells.
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