Fas ligand expression on T cells is sufficient to prevent prolonged airway inflammation in a murine model of asthma

Jiankun Tong, Bryan S. Clay, Caroline M. Ferreira, Hozefa S. Bandukwala, Tamson V. Moore, Kelly M. Blaine, Jesse W. Williams, Lisa M. Hoffman, Kimm J. Hamann, Rebecca A. Shilling, Joel V. Weinstock, Anne I. Sperling

Research output: Contribution to journalArticlepeer-review

6 Scopus citations

Abstract

Our previous studies revealed that, in a murine model of asthma, mice that received Fas-deficient T cells developed a prolonged phase of airway inflammation, mucus production, and airway hyperreactivity that failed to resolve even 6 weeks after the last challenge. To investigate how Fas-Fas ligand (FasL) interaction occurs between T cells and other cells in vivo, Gld mice with abnormalities of the FasL signaling pathway were used. The reconstituted mice were made by transferring T cells from B6 or Gld mice to Rag-/- or FasL-deficient Rag-/- mice. We found that Rag-/- mice that received B6 T cells resolved the airway inflammation, whereas FasL-deficient Rag-/- mice that received Gld T cells developed a prolonged airway inflammation at Day 28, with decreased IFN-γ production. Both FasL-deficient Rag-/- mice that received B6 T cells and Rag -/- mice that received Gld T cells also had completely resolved their airway inflammation by Day 28 after challenge. Interestingly, FasL-deficient Rag-/- mice that received Gld T cells eventually resolved airway inflammation at Day 42, with a similar level of IFN-γ production to that of control group. These results demonstrate that FasL expression on either T cells only or non-T cells only was sufficient for the eventual resolution of airway inflammation, and the prolonged airway inflammation in FasL-deficient Rag-/- mice that received Gld T cells was correlated with decreased IFN-γ production by Gld T cells.

Original languageEnglish (US)
Pages (from-to)342-348
Number of pages7
JournalAmerican journal of respiratory cell and molecular biology
Volume43
Issue number3
DOIs
StatePublished - Sep 1 2010
Externally publishedYes

Keywords

  • Apoptosis
  • Eosinophils
  • Inflammation
  • Lung
  • T helper cell type 1/T helper cell type 2 cells

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