Graft-versus-host reactions across different regions of the H-2 complex of the mouse.
Graft-versus-host reactions across different regions of the H-2 complex of the mouse.
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DOI：
10.1084/jem.137.5.1213
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发表时间：
1973-05-01
期刊：
影响因子：
--
通讯作者：
Park JM
中科院分区：
文献类型：
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作者：
Klein J;Park JM
H-2 交换及其亲本品系被排列成 35 种组合，其中成年脾细胞供体与新生受体在整个 H-2 复合体或复合体的三个、两个或一个区域中存在差异。然后使用西蒙森脾肿大测定来测试各个 H-2 区域对移植物抗宿主反应 (GVHR) 的贡献。结果表明最强的 GVHR 与 Ir 区域相关。 Ir区域的差异引起了显着的脾肿大，尽管迄今为止通过常规血清学方法尚未检测到与该区域相关的抗原。 K 区和 D 区的差异仅对 GVHR 产生临界影响，尽管事实上这些区域编码大多数（如果不是全部）可通过常规血清学和移植方法检测到的抗原。单独的K区域引起的GVHR并不比单独的D军团更强；然而，K + Ir 区域差异导致 GVHR 比 D 区域差异强得多。 Ss-Slp 区域也仅显示出对 GVHR 的边缘效应。两个或多个 H-2 区域的差异通常比每个区域单独的差异导致更大的脾肿大。基于这些发现得出的结论是，最强的 GVHR 是由与 H-2 复合物的已知组织相容性基因不同的基因引起的。据推测，GVHR基因与混合淋巴细胞反应(MLR)和Ir基因相同，并且这些基因的产物是胸腺来源的淋巴细胞(T细胞)表面的受体。
H-2 crossovers and their parental strains were arranged into 35 combinations in which the adult donor of spleen cells differed from the newborn recipient in the whole H-2 complex, or in three, two, or one region of the complex. A Simonsen splenomegaly assay was then used to test the contribution of the individual H-2 regions to the graft-versus-host reaction (GVHR). It was shown that the strongest GVHR was associated with the Ir region. Differences in the Ir region caused significant splenomegaly in spite of the fact that no antigens detectable by conventional serological methods have thus far been associated with this region. Differences in the K and D regions showed only a borderline effect on GVHR in spite of the fact that these regions code for most, if not all, of the antigens detectable by conventional serological and transplantation methods. The K region alone caused no stronger GVHR than the D legion alone; however, K + Ir region differences led to much stronger GVHR than D region differences. The Ss-Slp region also showed only a borderline effect on GVHR. Differences in two or more H-2 regions usually caused greater splenomegaly than differences in each of the regions separately. On the basis of these findings it is concluded that the strongest GVHR is caused by genes distinct from the known histocompatibility genes of the H-2 complex. It is speculated that the GVHR genes are identical with the mixed lymphocyte reaction (MLR) and Ir genes and that the product of these genes are receptors on the surface of the thymus-derived lymphocytes (T cells).