Ontogeny of RORγt cells in the intestine of newborns and its role in the development of experimental necrotizing enterocolitis.

Cell Biosci

Research Center of Translational Medicine, Shanghai Children's Hospital, Shanghai Institute of Immunology, State Key Laboratory of Oncogenes and Related Genes, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Published: January 2022

AI Article Synopsis

  • Neonates have an immature immune system that can lead to diseases like necrotizing enterocolitis (NEC), a severe condition primarily affecting premature infants.
  • A study on newborn mice found that a significant number of RORγt cells, involved in inflammatory responses, are present in their intestines during the first week of life.
  • Blocking RORγt activity with a specific antagonist reduced inflammation and improved NEC symptoms, suggesting these cells may play a crucial role in the disease's development.

Article Abstract

Background: Neonates possess an immature and plastic immune system, which is a major cause of some diseases in newborns. Necrotizing enterocolitis (NEC) is a severe and devastating intestinal disease that typically affects premature infants. However, the development of intestinal immune cells in neonates and their roles in the pathological process of NEC have not been elucidated.

Results: We examined the ontogeny of intestinal lamina propria lymphocytes in the early life of mice and found a high percentage of RORγt cells (containing inflammatory Th17 and ILC3 populations) during the first week of life. Importantly, the proportion of RORγt cells of intestinal lamina propria further increased in both NEC mice and patients tissue than the control. Furthermore, the application of GSK805, a specific antagonist of RORγt, inhibited IL-17A release and ameliorated NEC severity.

Conclusions: Our data reveal the high proportion of RORγt cells in newborn mice may directly contribute to the development of NEC.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8725364PMC
http://dx.doi.org/10.1186/s13578-021-00739-6DOI Listing

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