| First Author | Santori FR | Year | 2001 |
| Journal | J Immunol | Volume | 166 |
| Issue | 9 | Pages | 5416-21 |
| PubMed ID | 11313378 | Mgi Jnum | J:124752 |
| Mgi Id | MGI:3722499 | Doi | 10.4049/jimmunol.166.9.5416 |
| Citation | Santori FR, et al. (2001) Modulation of CD8+ T cell response to antigen by the levels of self MHC class I. J Immunol 166(9):5416-21 |
| abstractText | The response of H-Y-specific TCR-transgenic CD8(+) T cells to Ag is characterized by poor proliferation, cytolytic activity, and IFN-gamma secretion. IFN-gamma secretion, but not cytotoxic function, can be rescued by the B7.1 molecule, suggesting that costimulation can selectively enhance some, but not all, effector CD8(+) T cell responses. Although the H-Y epitope binds H-2D(b) relatively less well than some other epitopes, it can induce potent CTL responses in nontransgenic mice, suggesting that the observed poor responsiveness of transgenic CD8(+) T cells cannot be ascribed to the epitope itself. Previously reported reactivity of this TCR to H-2A(b) is also not the cause of the poor responsiveness of the H-Y-specific CD8(+) T cells, as H-Y-specific CD8(+) T cells obtained from genetic backgrounds lacking H-2A(b) also responded poorly. Rather, reducing the levels of H-2(b) class I molecules by breeding the mice to (C57BL/6 x B10.D2)F(1) or TAP1(+/-) backgrounds partially restored cytotoxic activity and enhanced proliferative responses. These findings demonstrate that the self MHC class I gene dosage may regulate the extent of CD8(+) T cell responsiveness to Ag. |
