Hemopoietic histocompatibility (Hh-1) phenotype and the regulation of its expression.
Hemopoietic histocompatibility (Hh-1) phenotype and the regulation of its expression.
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造血组织相容性（Hh-1）表型及其表达的调节。
DOI：
10.1007/bf00189521
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发表时间：
1992
期刊：
影响因子：
3.2
通讯作者：
Nakamura,I
中科院分区：
文献类型：
--
作者：
Kaminsky,SG;Yoshida,MA;Milisauskas,VK;Nakamura,I
杂种抗性(HR)主要由h-2复合体内的造血组织相容性-1(HH-1)基因控制。HR是Hh-1控制的目标决定因素在纯合子亲本品系小鼠中的结果，而在杂合F1杂交小鼠中则是它们缺失的结果。为了探讨控制HH-1表型的机制，对亲本EL-4(C57BL/6起源，H-2b)和R1(C58起源，H-2k)的三个独立体细胞杂交无性系进行了研究。EL-4系为HH-1b阳性，对H-2b杂合子F1小鼠具有HR作用，而R1缺乏Hh-1球蛋白，对HR不敏感。在三个杂交克隆中，F263.2是HH-1b阳性的，而另外两个F262.2和F264.2是HH-1阴性的，根据这些细胞与抗性(C57BL/6×C3H)F1小鼠移植的亲本C57BL/6细胞的体内竞争能力来判断。三个克隆均表达H-2b H-2k类抗原，对激活的NK细胞的易感性相同，均携带四个17号染色体拷贝。然而Southern分析显示，克隆F263.2含有三个h-2b染色体拷贝和一个H-2k拷贝，而另外两个克隆分别携带亲本17号染色体的两个拷贝。这些结果表明，特定等位基因的相对拷贝数是HH-1表型的关键决定因素，这使得基因剂量假说和反式显性抑制假说都不能解释HH-1表型的非共显性表达。
Hybrid resistance (HR) is primarily controlled by the genes of the Hemopoietic histocompatibility-1 (Hh-1) locus within theH-2complex. HR is a consequence of theHh-1-controlled target determinants in homozygous parental strain mice and their absence in heterozygous F1hybrid mice. To examine the mechanism that controls the Hh-1 phenotype, three independent clones of somatic cell hybrids between parental lines EL-4 (C57BL/6 origin,H-2b) and R1 (C58 origin,H-2k) were studied. The line EL-4 is Hh-1b-positive and is subject to HR byH-2bheterozygous F1mice, but R1 lacks theHh-1ballele and is not susceptible to HR. Of the three hybrid clones, F263.2 is Hh-1b-positive, whereas the other two, F262.2 and F264.2, are Hh-1-negative, as judged by these cells' capacity to compete in vivo with the grafted parental C57BL/6 bone marrow cells in the resistant (C57BL/6 × C3H)F1mice. All three clones express the H-2band H-2kclass I antigens equally well, are susceptible to activated NK cells to the same extent, and all carry four copies of chromosome 17. However, Southern analysis reveals that clone F263.2 contains three copies ofH-2bchromosome and oneH-2k, whereas the other two clones carry two copies each of the parental chromosome 17. The results suggest that the relative copy number of specific alleles is the crucial determinanr of the Hh-1 phenotype, and render unlikely both the gene dosage hypothesis and the trans-acting dominant suppression hypothesis to account for the noncodominant expression of the Hh-1 phenotype.