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Updated: Jun 23, 2025

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Prenatal inflammation remodels lung immunity and function by programming ILC2 hyperactivation.

Diego A López1, Aleah Griffin2, Lorena Moreno Aguilar3

  • 1Department of Pathology, University of Utah, Salt Lake City, UT, USA.

Cell Reports
|June 23, 2024
PubMed
Summary
This summary is machine-generated.

Prenatal inflammation, specifically maternal type I interferon, reprograms lung immune cells. This leads to hyperactivated innate lymphoid cells (ILC2s), increasing asthma susceptibility in offspring.

Keywords:
CP: ImmunologyILC2asthmadevelopmenthematopoiesishematopoietic stem celllungprenatal inflammationprogenitor

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Area of Science:

  • Immunology
  • Developmental Biology
  • Respiratory Medicine

Background:

  • Prenatal environmental exposures can significantly impact long-term health.
  • The developing lung's immune system is particularly vulnerable to early-life insults.
  • Group 2 innate lymphoid cells (ILC2s) play critical roles in lung immunity and tissue homeostasis.

Purpose of the Study:

  • To investigate how prenatal inflammation reprograms lung tissue immunity.
  • To identify the specific immune cells involved in this reprogramming process.
  • To elucidate the mechanisms linking prenatal inflammation to increased asthma susceptibility.

Main Methods:

  • Maternal type I interferon induction in a mouse model.
  • Analysis of immune cell populations in the developing and adult lung.
  • Adoptive transfer of fetal liver precursors.
  • Assessment of lung function and histopathology.

Main Results:

  • Maternal, but not fetal, type I interferon inflammation caused ILC2 expansion and hyperactivation.
  • Hyperactivated ILC2s produced increased IL-5 and IL-13, leading to Th2 bias and eosinophilia.
  • Prenatal inflammation reprogrammed fetal progenitors, causing persistent ILC2 hyperactivation and lung immune remodeling.
  • This remodeling increased asthma susceptibility, evidenced by worsened histopathology and airway dysfunction.

Conclusions:

  • Prenatal inflammation reprograms lung-resident ILC2s, establishing a pro-allergic immune environment.
  • Hyperactivated ILC2s driven by early-life inflammation are a key mechanism for increased asthma susceptibility.
  • Developmental programming of immune cells during the perinatal period has lasting consequences for lung health.