| First Author | Ford MS | Year | 2002 |
| Journal | J Exp Med | Volume | 196 |
| Issue | 2 | Pages | 261-7 |
| PubMed ID | 12119351 | Mgi Jnum | J:120698 |
| Mgi Id | MGI:3707663 | Doi | 10.1084/jem.20020029 |
| Citation | Ford MS, et al. (2002) The immune regulatory function of lymphoproliferative double negative T cells in vitro and in vivo. J Exp Med 196(2):261-7 |
| abstractText | Lymphoproliferative (lpr) mice, which lack functional Fas receptor expression and develop autoimmune lymphoproliferative disease, have an accumulation of T cell receptor-alphabeta(+)CD4(-)CD8(-) (double negative T cells [DNTC]) in the periphery. The function of the accumulating DNTC is not clear. In this study we demonstrate that B6/lpr DNTC can dose dependently kill syngeneic CD8(+) and CD4(+) T cells from wild-type B6 mice through Fas/Fas ligand interactions in vitro. We also demonstrate that B6/lpr DNTC that are activated and expand in vivo are able to specifically down-regulate allogeneic immune responses mediated by syngeneic Fas(+)CD4(+) and CD8(+) T cells in vivo. B6/lpr DNTC that have been preactivated in vivo by infusion of either class I- (bm1) or class II- (bm12) mismatched allogeneic lymphocytes are able to specifically enhance the survival of bm1 or bm12, but not third-party skin allografts when adoptively transferred into naive B6(+/+) mice. These findings clearly demonstrate that B6/lpr DNTC have a potent immune regulatory function in vitro and in vivo. They also provide new insights into the mechanisms involved in the development of autoimmune disease in lpr mice. |
