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 language | English (US) |
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Pages (from-to) | 342-348 |
Number of pages | 7 |
Journal | American journal of respiratory cell and molecular biology |
Volume | 43 |
Issue number | 3 |
DOIs | |
State | Published - Sep 1 2010 |
Externally published | Yes |
Keywords
- Apoptosis
- Eosinophils
- Inflammation
- Lung
- T helper cell type 1/T helper cell type 2 cells