| First Author | Céfai D | Year | 2001 |
| Journal | Int J Cancer | Volume | 91 |
| Issue | 4 | Pages | 529-37 |
| PubMed ID | 11251977 | Mgi Jnum | J:68509 |
| Mgi Id | MGI:1932791 | Doi | 10.1002/1097-0215(200002)9999:9999<::aid-ijc1074>3.0.co;2-o |
| Citation | Cefai D, et al. (2001) Role of Fas ligand expression in promoting escape from immune rejection in a spontaneous tumor model. Int J Cancer 91(4):529-37 |
| abstractText | Tumors escape immune-mediated rejection by a variety of mechanisms during tumor progression. The elucidation of these mechanisms in vivo suffers from a lack of suitable models of spontaneous tumor formation escaping active specific immunotherapy (ASI). In a rat neu transgenic (rNeu-TG) mouse model of spontaneous breast tumor formation, we showed that rNeu-TG mice developed late escape tumors despite the presence of a persistent rNeu-specific immune response after ASI. Cell suspensions derived from these escape tumors grew in vaccinated tumor-free mice, whereas injected spontaneous tumor cells were rejected. Escape tumors retained rNeu or MHC class I expression but significantly upregulated Fas (CD95, Apo-1) ligand. We further demonstrated that Fas-L on escape tumor cells correlated with apoptosis of infiltrating T lymphocytes. Thus, our results provide evidence that spontaneous breast tumors upregulate Fas-L expression after vaccination that may promote tumor escape in vivo after ASI. Copyright 2001 Wiley-Liss, Inc. |
