Autor: |
Cutting JA, Watanabe DH, Strebel FR, McBride RA |
Jazyk: |
angličtina |
Zdroj: |
Journal of immunogenetics [J Immunogenet] 1981 Jun; Vol. 8 (3), pp. 215-23. |
DOI: |
10.1111/j.1744-313x.1981.tb00759.x |
Abstrakt: |
Schmidt-Ruppin Rous sarcoma virus, subgroup B (SR-RSV-B), was inoculated into the wingwebs of chickens from three partially congenic inbred lines, G-B1, G-B2 and G-B3, homozygous for different MHC (B region) haplotypes (genotypes = B1/B1, B2/B2 and B3/B3 respectively). All birds developed tumours but only the G-B2 line resisted progressive tumour growth. Birds from lines G-B1 and G-B3 approached 100% susceptibility to progressive tumour growth, whereas most (G-B1 X G-B3) F1 hybrids were resistant to tumours induced by SR-RSV-B. The association of the resistance trait in F1 hybrids with genes of the B region was investigated by testing progeny of (G-B1 X G-B3) X B-B1 F1 and (G-B1 X G-B2) X G-B3 F1 backcross matings. Approximately 27% of the backcross population was resistant to SR-RSV-B-induced tumours and these resistant offspring were predominantly of the B1/B3 phenotype. We interpret these results to mean that resistance to progressive tumour growth involves complementation between genes (allelic or at separate loci) linked to or within the B region and that resistance is effective only when the complementing B region genes act in concert with complementing genes which assort independently of the MHC. We suggest that complementing B region-linked genes are homologues of complementing murine H-2-linked Ir genes. The function of the B region in determining growth of sarcomas may therefore be analogous to that of Ir genes. |
Databáze: |
MEDLINE |
Externí odkaz: |
|