Affordable Access

deepdyve-link
Publisher Website

IL-33-Responsive Group 2 Innate Lymphoid Cells Are Regulated by Female Sex Hormones in the Uterus.

Authors
  • Bartemes, Kathleen1, 2
  • Chen, Chien-Chang1, 2
  • Iijima, Koji1
  • Drake, Li1
  • Kita, Hirohito3, 2
  • 1 Division of Allergic Diseases, Department of Internal Medicine, Mayo Clinic, Rochester, MN 55905; and.
  • 2 Department of Immunology, Mayo Clinic, Rochester, MN 55905.
  • 3 Division of Allergic Diseases, Department of Internal Medicine, Mayo Clinic, Rochester, MN 55905; and [email protected]
Type
Published Article
Journal
The Journal of Immunology
Publisher
The American Association of Immunologists
Publication Date
Jan 01, 2018
Volume
200
Issue
1
Pages
229–236
Identifiers
DOI: 10.4049/jimmunol.1602085
PMID: 29133293
Source
Medline
License
Unknown

Abstract

Group 2 innate lymphoid cells (ILC2s) reside in multiple organs in the body, where they play roles in immunity, tissue homeostasis, and metabolic regulation. However, little is known about the regulatory mechanisms of ILC2s in different organs. Here, we identified ILC2s in the mouse uterus and found that they express cell surface molecules, including the IL-33 receptor, ST2, that are roughly comparable to those expressed by lung ILC2s. Both in vivo and in vitro treatment with IL-33 induced type 2 cytokine production in uterine ILC2s, suggesting that they respond to IL-33 in a manner similar to ILC2s in other organs. Importantly, uterine ILC2s were nearly absent in ovariectomized mice and were increased in wild-type mice by estrogen administration, whereas lung ILC2s were unaffected by both ovariectomy and estrogen administration. Likewise, a marked reduction in uterine ILC2s was observed in mice deficient in estrogen receptor α or estrogen receptor β. Furthermore, uterine ILC2s highly expressed estrogen receptor α, and in vitro culture of isolated uterine ILC2s with 17β-estradiol modified expression of a number of genes. Finally, an increased prevalence in neonatal mortality was observed in litters from dams lacking the IL-33 receptor, ST2. Taken together, our findings indicate that unlike lung IL2Cs, uterine ILC2s are regulated by female sex hormones, which may specialize them for specific physiological functions.

Report this publication

Statistics

Seen <100 times