| First Author | Dutz JP | Year | 1995 |
| Journal | Immunology | Volume | 85 |
| Issue | 1 | Pages | 74-81 |
| PubMed ID | 7543449 | Mgi Jnum | J:25163 |
| Mgi Id | MGI:72892 | Citation | Dutz JP, et al. (1995) A mutation in the alpha 3 domain of Db that abrogates CD8 binding does not affect presentation of an immunodominant H-Y peptide. Immunology 85(1):74-81 |
| abstractText | The peptidic nature of the male (H-Y) antigen, a model minor histocompatibility antigen in H-2b mice, has recently been demonstrated. In this study we show that the H-Y peptide, which is recognized by PM-1, a Db-restricted cytotoxic T-lymphocyte (CTL) clone, is absent in male H-2d spleen cells but present in male H-2d spleen cells that also express a transgenic Db molecule under its endogenous promoter. This result indicates that both the H-Y and the Db gene products are essential and sufficient for production of the Db-restricted H-Y peptide. By comparing the ability of the PM-1 clone and bulk CTL generated in a secondary mixed lymphocyte culture to recognize H-Y peptidic material eluted from affinity-purified Db molecules and separated by reversed-phase high-performance liquid chromatography (HPLC), we provide evidence that there is an immunodominant H-Y epitope that is presented by the Db molecule. Furthermore, the presentation of this epitope is not affected by a mutation in the alpha 3 domain of Db (asp227 to lys227), which abrogates CD8 binding, since similar amounts of H-Y peptide were eluted from affinity-purified wild-type or mutant Db molecules. However, the generation of the H-Y epitope is dependent on the presence of beta 2-microglobulin, since it is absent in male H-2b mice that lack a functional beta 2-microglobulin gene. The implications of these findings on T-cell development are discussed. |
