McCullagh P
Scand J Immunol. 1977;6(10):981-9. doi: 10.1111/j.1365-3083.1977.tb00333.x.
The subpopulation of parental-strain lymphocytes responsible for the recognition of a particular F1 hybrid strain as foreign has been shown to be subject to specific, reversible inactivation after its injection into neonatal rats of that F1 hybrid strain. Neonates born to mothers that were syngeneic with the parental-strain lymphocytes under test acquired the capacity to inactivate these lymphocytes at an earlier age than did the genotypically identical reciprocal F1 hybrids. Neonates had little capacity to inactivate completely allogeneic lymphocytes. It is inferred from the difference in behavior between reciprocal F1 hybrids that the augmented ability to inactivate anti-F1 hybrid maternal-strain lymphocytes follows exposure to such cells in utero and to antibodies with anti-F1 hybrid activity in colostrum. Specific inactivation of those marauding maternal lymphocytes with anti-fetal activity is envisaged as an important means of protection of the fetus from immunological attack by the mother. On the basis of the results presented in this and the preceding paper, it has been proposed that many of the sequelae of the transfer of immunocompetent parental-strain cells to F1 hybrid animals result not from graft anti-host activity but from an F1 hybrid anti-parental lymphocyte response that has eluded normal regulatory mechanisms. These experiments also raise the possibility that regulation of auto-immune responses may be achieved by the inactivation of lymphocytes with anti-self reactivity by other lymphocytes that respond to the recognition structure required for such reactivity.
负责将特定F1杂交品系识别为外来品系的亲本品系淋巴细胞亚群,在注入该F1杂交品系的新生大鼠体内后,已被证明会受到特异性、可逆性失活。与受试亲本品系淋巴细胞同基因的母亲所生的新生儿,比基因相同的反向F1杂交品系在更早的年龄就获得了使这些淋巴细胞失活的能力。新生儿完全灭活异基因淋巴细胞的能力很弱。从反向F1杂交品系行为的差异可以推断,灭活抗F1杂交品系母体淋巴细胞的能力增强是由于在子宫内接触了此类细胞以及在初乳中接触了具有抗F1杂交活性的抗体。设想特异性灭活那些具有抗胎儿活性的母体掠夺性淋巴细胞是保护胎儿免受母亲免疫攻击的重要手段。根据本文及前文给出的结果,有人提出,将具有免疫活性的亲本品系细胞转移到F1杂交动物体内产生的许多后遗症,并非源于移植物抗宿主活性,而是源于F1杂交品系对亲本品系淋巴细胞的反应,这种反应避开了正常的调节机制。这些实验还提出了一种可能性,即自身免疫反应的调节可能是通过具有抗自身反应性的淋巴细胞被其他对这种反应所需识别结构有反应的淋巴细胞失活来实现的。