Woodland D, Happ M P, Bill J, Palmer E
Division of Basic Sciences, National Jewish Center for Immunology and Respiratory Medicine, Denver, CO 80206.
Science. 1990 Feb 23;247(4945):964-7. doi: 10.1126/science.1968289.
T cells that express the T cell receptor V beta 5.2 domain react with the class II major histocompatibility complex (MHC) molecule I-E, and V beta 5.2+ T cells are deleted in mouse strains that express I-E glycoproteins. By examination of genetically defined recombinant inbred (RI) mouse strains, it was found that the deletion was dependent on the expression of I-E and one of a limited number of non-MHC gene products (cotolerogens). The gene encoding one of these cotolerogens maps to chromosome 12 and is linked to the endogenous provirus Mtv-9. These observations suggest that the I-E-mediated and minor lymphocyte-stimulating antigen (Mls)-mediated deletions of alpha beta T cells from the repertoire are similar; both require the expression of a class II MHC glycoprotein and a second non-MHC gene product.
表达T细胞受体Vβ5.2结构域的T细胞与II类主要组织相容性复合体(MHC)分子I-E发生反应,并且在表达I-E糖蛋白的小鼠品系中Vβ5.2+T细胞会被清除。通过对基因定义的重组近交(RI)小鼠品系进行检测,发现这种清除依赖于I-E以及有限数量的非MHC基因产物(共同耐受原)之一的表达。编码这些共同耐受原之一的基因定位于12号染色体,并且与内源性前病毒Mtv-9连锁。这些观察结果表明,I-E介导的以及微小淋巴细胞刺激抗原(Mls)介导的αβT细胞从库中清除是相似的;两者都需要II类MHC糖蛋白和第二种非MHC基因产物的表达。