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Proc Natl Acad Sci U S A. 2007 Dec 18;104(51):20460-5. Epub 2007 Dec 11.

Evasion of myofibroblasts from immune surveillance: a mechanism for tissue fibrosis.

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  • 1Lung Cellular and Molecular Biology Laboratory, Institute of Pulmonary Medicine Hadassah, Hebrew University Medical Center, Jerusalem 91120, Israel.


Tissue fibrosis evolving from impaired tissue remodeling after injury is characterized by myofibroblast accumulation. We propose that during the development of fibrosis myofibroblasts acquire an immune-privileged cell phenotype, allowing their uninterrupted accumulation. Using the murine model of bleomycin-induced lung fibrosis in mice, we show that myofibroblasts that accumulate in lungs with fibrosis, but not in normal lungs, kill Fas(+) lymphocytes, resist Fas-induced apoptosis, and survive longer when grafted into allogeneic mice. In contrast, bleomycin-treated FasLigand (FasL)-deficient (gld) chimeric mice did not accumulate myofibroblasts or collagen in their lungs, and their FasL(-) myofibroblasts did not survive after alloengraftment. This finding indicates that myofibroblasts possess Fas/FasL-pathway-dependent characteristics that allow them to escape from immune surveillance and resulting organ fibrosis.

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