www.nature.com/mi COMMENT A pulmonary ILC3 niche promotes neonatal mucosal immunity to respiratory bacterial infection and is associated with postnatal lung development 1,2 Malcolm R. Starkey Mucosal Immunology (2020) 13:385–387; https://doi.org/10.1038/s41385-020-0283-9 The importance of innate lymphoid cell (ILC) interactions with addition, the impacts of early life ILC3 priming by infection or stromal cells in discrete tissues niches is emerging as a key premature birth on susceptibility to chronic lung diseases in later- regulator of homeostasis and repair. A recent study by Oherle life is unknown and requires further exploration. et al., extends this phenomenon to developmental processes, showing that ILC progenitors seed the neonatal lung and respond to alveolar ﬁbroblast-derived insulin-like growth factor 1 (IGF1) to ILC PRECURSORS GIVE RISE TO MATURE ILC3 IN THE promote group 3 ILC (ILC3) biogenesis linking postnatal lung NEONATAL LUNG AND PROTECT AGAINST RESPIRATORY S. maturation with the development of mature pulmonary ILC3 and PNEUMONIAE INFECTION lung mucosal defenses. They show that premature human infants It has been shown previously that pulmonary ILC subsets, and mice with experimental bronchopulmonary dysplasia (BPD), particularly group 2 ILC (ILC2), expand rapidly in the developing 4,5 have reduced IGF1 and ILC3 resulting in increased susceptibility to postnatal mouse
Mucosal Immunology – Springer Journals
Published: May 17, 2020
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