Marusić-Galesić S, Walden P
Department of Molecular Medicine, Instituté Ruder Boskovic, Zabreb, Croatia.
Immunology. 1995 Jul;85(3):442-6.
Targeted disruption of the A beta-encoding gene of H2b mice abolishes major histocompatibility complex (MHC) class II expression and results in a failure to develop CD4+8- T cells. Besides this major effect, the lack of class II expression affects the level of T-cell receptor (TCR) and CD4 expression on differentiating thymocytes. Moreover, there is no class II-mediated negative selection of thymocytes. All this could result in TCR repertoire changes of the CD4-8+ T-cell subpopulation, which apparently develops normally in these mice. To test this hypothesis, the class II reactivity of CD4-8+ T cells from class II-deficient (class II0) mice was analysed. It was found that CD4-8+ T cells from class II0 but not from class II-expressing mice developed a significant level of cytotoxicity against class II-expressing target cells. These results demonstrate an influence of MHC class II molecules on the TCR repertoire of CD4-8+ T cells.
对H2b小鼠的β淀粉样蛋白编码基因进行靶向破坏,会消除主要组织相容性复合体(MHC)II类表达,并导致CD4+8-T细胞发育失败。除了这一主要影响外,II类表达的缺失还会影响分化中的胸腺细胞上T细胞受体(TCR)和CD4表达的水平。此外,不存在II类介导的胸腺细胞阴性选择。所有这些都可能导致CD4-8+T细胞亚群的TCR库发生变化,而该亚群在这些小鼠中显然发育正常。为了验证这一假设,分析了来自II类缺陷(II类0)小鼠的CD4-8+T细胞的II类反应性。结果发现,来自II类0小鼠而非表达II类的小鼠的CD4-8+T细胞,对表达II类的靶细胞产生了显著水平的细胞毒性。这些结果证明了MHC II类分子对CD4-8+T细胞TCR库的影响。