Non-apoptotic fas (CD95) signaling on T cells regulates the resolution of Th2-mediated inflammation

Jesse W. Williams, Caroline M. Ferreira, Kelly M. Blaine, Crystal Rayon, Francisco Velázquez, Jiankun Tong, Marcus E. Peter, Anne I. Sperling*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

11 Scopus citations


Fas (CD95/APO-1) and its ligand (FasL/CD95L) promote the resolution of type 2 lung inflammation and eosinophilia. We previously found that Fas-deficiency on T cells, but not eosinophils, delayed resolution of inflammation. However, Fas can signal both cell death and have a positive signaling function that can actually activate cells. In this study, we investigated whether Fas-induced death or Fas-activated signaling pathways promote resolution of allergic lung inflammation. By increasing T cell survival through two Fas-independent pathways, using Bim-deficient T cells or Bcl-xL overexpressing T cells, no differences in resolution of Th2-mediated inflammation was observed. Furthermore, Th2 cells were inherently resistant to Fas-mediated apoptosis and preferentially signaled through non-apoptotic pathways following FasL treatment. Utilizing Fas-mutant mice deficient in apoptotic but sufficient for non-apoptotic Fas signaling pathways, we demonstrate that non-apoptotic Fas signaling in T cells drives resolution of Th2-mediated airway inflammation. Our findings reveal a previously unknown role for non-apoptotic Fas signaling on Th2 cells in the induction of resolution of type 2 inflammation.

Original languageEnglish (US)
Article number2521
JournalFrontiers in immunology
Issue numberNOV
StatePublished - Nov 1 2018


  • Allergy
  • Apoptosis
  • Asthma
  • Eosinophilia
  • Fas-FasL
  • Th2 cells

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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