| First Author | Seino K | Year | 1996 |
| Journal | Int Immunol | Volume | 8 |
| Issue | 9 | Pages | 1347-54 |
| PubMed ID | 8921411 | Mgi Jnum | J:42521 |
| Mgi Id | MGI:1095945 | Doi | 10.1093/intimm/8.9.1347 |
| Citation | Seino K, et al. (1996) Contribution of Fas ligand to cardiac allograft rejection. Int Immunol 8(9):1347-54 |
| abstractText | Effector mechanisms for allograft injury remain unclear. In the present study, we verified the contribution of Fas and Fas ligand (FasL) to cardiac allograft rejection by utilizing the Fas-deficient lpr or FasL-deficient gld mice as the donor or recipient. Cardiac myocytes prepared from normal mice, but not those from lpr mice, constitutively expressed Fas and were susceptible to FasL-mediated lysis. Survival of cardiac allografts was substantially prolonged when gld or lpr mice were used as the recipient. In contrast, cardiac allografts from lpr mice were normally rejected without a delay. Histological examination of the grafts in the gld or lpr recipients demonstrated a lesser cellular infiltration and much milder myocyte damage. Proliferative response and cytotoxic T lymphocyte induction against the donor-type alloantigens were not impaired in the gld or lpr recipients. These results indicate a substantial contribution of FasL to cardiac allograft rejection, independent of Fas in the grafts. This ralses a possibility that FasL may be more generally involved in tissue damage associated with various diseases than expected from the expression of Fas in the target organs. |
