Drizlikh G, Schmidt-Sole J, Yankelevich B
J Exp Med. 1984 Apr 1;159(4):1070-82. doi: 10.1084/jem.159.4.1070.
Irradiated (H-2b X H-2k)F1 and (H-2b X H-2d)F1 recipients strongly resist the growth of H-2b parental bone marrow cells and do not resist marrow grafts from non-H-2b parents such as C3H and BALB/c. This phenomenon of hybrid resistance has been shown to be under genetic control of the H-2D-linked loci and was interpreted by Cudkowicz (9) as due to the existence of H-2D-linked recessive hemopoietic histocompatibility genes. To check whether the H-2D-linked loci are solely responsible for the fate of bone marrow allografts, we measured the strength of resistance of irradiated (B6 X C3H)F1 and (B6 X BALB/c)F1 recipients toward bone marrow grafts from a set of H-2 recombinant and F1 hybrid donors carrying either the H-2b, H-2d, and H-2k alleles. We found that growth of all H-2b grafts was resisted, although to different degrees. Resistance was minimal when donors shared with the input strain of a corresponding F1 hybrid the H-2K and H-2I regions, or when both F1 donors and F1 recipients formed identical unique hybrid Ia molecules. In addition, H-2b grafts were resisted by congenic, H-2D-identical, H-2K-and H-2I-incompatible recipients. The fate of grafts from H-2Dd donors seemed to depend on the incompatibility of the combinatorial determinant Ia.22. If both donor and recipient expressed such a determinant (either in the cis or in the transposition), or if neither could form such a determinant, grafts were not resisted. The H-2Dk allele is not the main or only factor that confers on the C3H parental bone marrow cells the ability to grow unresisted in (B6 X C3H)F1 recipients. Grafts from congenic C3H.OH donors, carrying the same H-2Dk alleles and differing in the left part of the H-2 complex, were resisted by the F1 recipients. We conclude that both class I (K and D) and class II (I-A and I-E) major histocompatibility complex genes, rather than hypothetical hemopoietic histocompatibility genes control hemopoietic resistance. To reconcile codominant inheritance of classic H-2 antigens with the apparent recessive inheritance of hybrid resistance, we assume that there exist parental determinants that are not formed in some F1 hybrids due to preferential association of either Ia alpha chains with allogeneic beta chains or of class I antigens with allogeneic or hybrid class II restriction elements.
受照射的（H-2b×H-2k）F1和（H-2b×H-2d）F1受体强烈抵抗H-2b亲本骨髓细胞的生长，而不抵抗来自非H-2b亲本如C3H和BALB/c的骨髓移植。这种杂种抗性现象已被证明受H-2D连锁基因座的遗传控制，Cudkowicz（9）将其解释为由于存在H-2D连锁的隐性造血组织相容性基因。为了检查H-2D连锁基因座是否是骨髓同种异体移植命运的唯一决定因素，我们测量了受照射的（B6×C3H）F1和（B6×BALB/c）F1受体对来自一组携带H-2b、H-2d和H-2k等位基因的H-2重组体和F1杂种供体的骨髓移植的抵抗强度。我们发现，所有H-2b移植的生长都受到抵抗，尽管程度不同。当供体与相应F1杂种的输入菌株共享H-2K和H-2I区域时，或者当F1供体和F1受体都形成相同的独特杂种Ia分子时，抵抗最小。此外，同基因、H-2D相同、H-2K和H-2I不兼容的受体也抵抗H-2b移植。来自H-2Dd供体的移植命运似乎取决于组合决定簇Ia.22的不兼容性。如果供体和受体都表达这样的决定簇（顺式或反式），或者如果两者都不能形成这样的决定簇，则移植不会受到抵抗。H-2Dk等位基因不是赋予C3H亲本骨髓细胞在（B6×C3H）F1受体中无抵抗生长能力的主要或唯一因素。携带相同H-2Dk等位基因且H-2复合体左半部分不同的同基因C3H.OH供体的移植受到F1受体的抵抗。我们得出结论，I类（K和D）和II类（I-A和I-E）主要组织相容性复合体基因，而不是假设的造血组织相容性基因控制造血抗性。为了使经典H-2抗原的共显性遗传与杂种抗性的明显隐性遗传相协调，我们假设存在亲本决定簇，由于Iaα链与同种异体β链或I类抗原与同种异体或杂种II类限制元件的优先结合，在某些F1杂种中不形成这些决定簇。
