| First Author | Roopenian DC | Year | 1993 |
| Journal | J Immunol | Volume | 151 |
| Issue | 9 | Pages | 4595-605 |
| PubMed ID | 8409421 | Mgi Jnum | J:15218 |
| Mgi Id | MGI:63347 | Doi | 10.4049/jimmunol.151.9.4595 |
| Citation | Roopenian DC, et al. (1993) The functional basis of minor histocompatibility loci. J Immunol 151(9):4595-605 |
| abstractText | This work addresses the functional basis of classical minor histocompatibility (H) loci. We focus on the H-3 locus, which is actually a complex genetic unit to which the phenotypic trait of tissue rejection, genes whose products stimulate specific subsets of T cells, and Ir genes have been mapped. To clarify how these genes relate to one another and to the trait of tissue rejection, strains of intra-H-3 recombinant mice were produced and analyzed. These mice allowed us to selectively elicit immune responses to Ag (referred to as type I Ag) that stimulate MHC class I-restricted CTL, or Ag (referred to as type II Ag) that stimulate MHC class II-restricted Th. The splitting of H-3 in this manner resulted in a dramatic diminution of the skin allograft response, and with rare exception, an elimination of the CTL response after spleen cell immunization. A selective response to type I Ag resulted in slow, incomplete skin allograft rejection that demonstrated both CD4+ cell-dependent and -independent components. A selective response to the type II Ag failed to result in allograft rejection. The type II Ag did, however, act as an Ir gene that determined whether responses to type I Ag could occur. Altogether, the results indicate that the trait of tissue rejection associated with H-3 is a consequence of the strongly synergistic effects of Th-CTL collaboration induced by products of type I and type II genes. Moreover, the results suggest a genetic explanation for some of the Ir gene effects associated with H-3. |
