Nowinski R C
Infect Immun. 1976 Apr;13(4):1098-102. doi: 10.1128/iai.13.4.1098-1102.1976.
Humoral immune response to ectropic leukemia viruses in AKR and C57BL/6 mice was controlled by a gene that mapped in linkage group IX. Mice of the AKR strain had an immune nonresponsive allele of this gene, whereas mice of the C57BL/6 strain had an immune responsive allele. Antibody against murine leukemia virus (MuLV) reacted primarily with p15 protein of the viral envelope. It was concluded that the failure to find antibody production in AKR mice was the result of a genetic immunological defect, rather than the result of immunological tolerance that was induced by the persistent viremia of endogenous MuLV.
AKR和C57BL/6小鼠对外源白血病病毒的体液免疫反应受位于第九连锁群的一个基因控制。AKR品系的小鼠具有该基因的免疫无反应等位基因,而C57BL/6品系的小鼠具有免疫反应等位基因。抗鼠白血病病毒(MuLV)抗体主要与病毒包膜的p15蛋白发生反应。得出的结论是,在AKR小鼠中未能发现抗体产生是遗传免疫缺陷的结果,而不是内源性MuLV持续病毒血症诱导的免疫耐受的结果。