| First Author | Borges VM | Year | 2001 |
| Journal | J Exp Med | Volume | 194 |
| Issue | 2 | Pages | 155-64 |
| PubMed ID | 11457890 | Mgi Jnum | J:118034 |
| Mgi Id | MGI:3698374 | Doi | 10.1084/jem.194.2.155 |
| Citation | Borges VM, et al. (2001) Fas ligand triggers pulmonary silicosis. J Exp Med 194(2):155-64 |
| abstractText | We investigated the role of Fas ligand in murine silicosis. Wild-type mice instilled with silica developed severe pulmonary inflammation, with local production of tumor necrosis factor (TNF)-alpha, and interstitial neutrophil and macrophage infiltration in the lungs. Strikingly, Fas ligand-deficient generalized lymphoproliferative disease mutant (gld) mice did not develop silicosis. The gld mice had markedly reduced neutrophil extravasation into bronchoalveolar space, and did not show increased TNF-alpha production, nor pulmonary inflammation. Bone marrow chimeras and local adoptive transfer demonstrated that wild-type, but not Fas ligand-deficient lung macrophages recruit neutrophils and initiate silicosis. Silica induced Fas ligand expression in lung macrophages in vitro and in vivo, and promoted Fas ligand-dependent macrophage apoptosis. Administration of neutralizing anti-Fas ligand antibody in vivo blocked induction of silicosis. Thus, Fas ligand plays a central role in induction of pulmonary silicosis. |
