IL-33 activates group 2 innate lymphoid cell expansion and modulates endometriosis.

Journal Article (Journal Article)

Chronic inflammation and localized alterations in immune cell function are suspected to contribute to the progression of endometriosis and its associated symptoms. In particular, the alarmin IL-33 is elevated in the plasma, peritoneal fluid, and endometriotic lesions from patients with endometriosis; however, the exact role of IL-33 in the pathophysiology of endometriosis is not well understood. In this study, we demonstrate, in both humans and a murine model, that IL-33 contributes to the expansion of group 2 innate lymphoid cells (ILC2s), and this IL-33-induced ILC2 expansion modulates the endometriosis lesion microenvironment. Importantly, we show that IL-33 drives hallmarks of severe endometriosis, including elevated inflammation, lesion proliferation, and fibrosis, and that this IL-33-induced aggravation is mediated by ILC2s. Finally, we demonstrate the functionality of IL-33 neutralization as a promising and potentially novel therapeutic avenue for treating the debilitating symptoms of endometriosis.

Full Text

Duke Authors

Cited Authors

  • Miller, JE; Lingegowda, H; Symons, LK; Bougie, O; Young, SL; Lessey, BA; Koti, M; Tayade, C

Published Date

  • December 8, 2021

Published In

Volume / Issue

  • 6 / 23

PubMed ID

  • 34699382

Pubmed Central ID

  • PMC8675188

Electronic International Standard Serial Number (EISSN)

  • 2379-3708

Digital Object Identifier (DOI)

  • 10.1172/jci.insight.149699


  • eng

Conference Location

  • United States