| First Author | Wallach-Dayan SB | Year | 2007 |
| Journal | Proc Natl Acad Sci U S A | Volume | 104 |
| Issue | 51 | Pages | 20460-5 |
| PubMed ID | 18077384 | Mgi Jnum | J:130580 |
| Mgi Id | MGI:3771930 | Doi | 10.1073/pnas.0705582104 |
| Citation | Wallach-Dayan SB, et al. (2007) Evasion of myofibroblasts from immune surveillance: a mechanism for tissue fibrosis. Proc Natl Acad Sci U S A 104(51):20460-5 |
| abstractText | 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. |
