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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. wallach-dayan@hadassah.org.il

Abstract

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.

PMID:
18077384
[PubMed - indexed for MEDLINE]
PMCID:
PMC2154453
Free PMC Article
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