Sakai T, Agui T, Muramatsu Y, Yamada T, Hisaeda H, Himeno K, Matsumoto K
Department of Parasitology and Immunology, University of Tokushima School of Medicine, Japan.
J Vet Med Sci. 1996 Nov;58(11):1125-7. doi: 10.1292/jvms.58.11_1125.
Long-Evans Cinnamon (LEC) rats show a novel maturational arrest from CD4+8+ to CD4+8- thymocytes but a cause of this mutation is not identified. The candidate for this mutation is a defect in the function of CD4 or major histocompatibility complex (MHC) class II because gene-disrupted mice defective for CD4 or MHC class II molecules show a specific defect in CD4+ T cells. Previously, we showed that MHC class II is not a cause of this maturational arrest. Therefore, in this study, we focus on the function of CD4 molecules in LEC rat thymocytes. CD4 molecules on LEC rat thymocytes associated with protein tyrosine kinase, p56[lck], normally. Furthermore, cross-linking of CF4 molecules by anti-rat CD4 mAb elicited the elevation of intracellular calcium concentrations ([Ca2+]i) in LEC rat thymocytes, suggesting that CD4 molecules can deliver the signal normally. These results indicate that function of CD4 is normal and the maturational blockade of CD4+8- thymocytes in LEC rats is not caused by specific lymphocyte molecules that have been shown in gene-disrupted mice.
长-伊文斯肉桂色(LEC)大鼠表现出从CD4⁺8⁺胸腺细胞到CD4⁺8⁻胸腺细胞的一种新型成熟停滞,但该突变的原因尚未确定。此突变的候选因素是CD4或主要组织相容性复合体(MHC)II类功能缺陷,因为CD4或MHC II类分子基因敲除的小鼠在CD4⁺T细胞中表现出特定缺陷。此前,我们表明MHC II类不是这种成熟停滞的原因。因此,在本研究中,我们聚焦于LEC大鼠胸腺细胞中CD4分子的功能。LEC大鼠胸腺细胞上的CD4分子通常与蛋白酪氨酸激酶p56[lck]相关。此外,抗大鼠CD4单克隆抗体对CF4分子的交联引发了LEC大鼠胸腺细胞内钙浓度([Ca²⁺]i)的升高,表明CD4分子能够正常传递信号。这些结果表明CD4功能正常,LEC大鼠中CD4⁺8⁻胸腺细胞的成熟阻滞不是由基因敲除小鼠中已显示的特定淋巴细胞分子引起的。