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Published ahead of print on October 23, 2009
Am. J. Respir. Cell Mol. Biol. 2009, doi:10.1165/rcmb.2008-0454OC
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Submitted on November 22, 2008
Accepted on October 22, 2009

FasL Expression on T Cells is Sufficient to Prevent Prolonged Airway Inflammation in a Murine Model of Asthma

Jiankun Tong1*, Bryan S Clay2, Caroline M Ferreira3, Hozefa S Bandukwala4, Tamson V Moore4, Kelly M Blaine3, Jesse W Williams5, Lisa M Hoffman3, Kimm J Hamann6, Rebecca A Shilling2, Joel V Weinstock7, and Anne I Sperling8

1 Section of Pulmonary and Critical Care Medicine, Department of Medicine, University of Chicago, Chicago, Illinois, United States; Department of Pathology, University of Chicago, Chicago, Illinois, United States, 2 Section of Pulmonary and Critical Care Medicine, Department of Medicine, University of Chicago, Chicago, Illinois, United States; Committee on Immunology, University of Chicago, Chicago, Illinois, United States, 3 Section of Pulmonary and Critical Care Medicine, Department of Medicine, University of Chicago, Chicago, Illinois, United States, 4 Committee on Immunology, University of Chicago, Chicago, Illinois, United States, 5 Pathology, University of Chicago, Chicago, Illinois, United States; Committee on Molecular Pathology and Molecular Medicine, University of Chicago, Chicago, Illinois, United States, 6 Section of Pulmonary and Critical Care Medicine, Department of Medicine, University of Chicago, Chicago, Illinois, United States; Committee on Molecular Pathology and Molecular Medicine, University of Chicago, Chicago, Illinois, United States, 7 Division of Gastroenterology/Hepatology, Department of Medicine, Tufts University, New England Medical Center, Boston, Massachusetts, United States, 8 Section of Pulmonary and Critical Care Medicine, Department of Medicine, University of Chicago, Chicago, Illinois, United States; Committee on Immunology, University of Chicago, Chicago, Illinois, United States; Committee on Molecular Pathology and Molecular Medicine, University of Chicago, Chicago, Illinois, United States

* To whom correspondence should be addressed. E-mail: jtong{at}medicine.bsd.uchicago.edu.

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-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, while FasL-deficient Rag-/- mice that received Gld T cells developed a prolonged airway inflammation at day 28 with decreased IFN{gamma} production. Both FasL-deficient Rag-/-mice that received B6 T cells and Rag-/- mice that received Gld T cells had also 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{gamma} production to that of control group. These results demonstrated 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{gamma} production by Gld T cells.


Key words: Th1/Th2 cells • Eosinophils • Apoptosis • Lung • inflammation






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