Impaired development of V gamma 3 dendritic epidermal T cells in p56lck protein tyrosine kinase-deficient and CD45 protein tyrosine phosphatase-deficient mice.
Impaired development of V gamma 3 dendritic epidermal T cells in p56lck protein tyrosine kinase-deficient and CD45 protein tyrosine phosphatase-deficient mice.
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DOI：
10.1084/jem.181.1.345
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发表时间：
1995-01-01
期刊：
影响因子：
--
通讯作者：
Ohashi PS
中科院分区：
文献类型：
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作者：
Kawai K;Kishihara K;Molina TJ;Wallace VA;Mak TW;Ohashi PS
为了确定p56 lck蛋白酪氨酸激酶和CD 45蛋白酪氨酸磷酸酶是否参与γ/δ T细胞胸腺内分化过程中的信号转导，我们研究了表达V γ 3 T细胞受体（TCR）的小鼠中任一蛋白缺陷的T细胞的发育。来自两只小鼠的皮肤含有显著减少数量的树突状表皮T细胞，所述树突状表皮T细胞在细胞表面表达降低水平的V γ 3 TCR。对这些小鼠的胎儿胸腺的分析表明，V γ 3胸腺细胞的成熟在未成熟阶段被阻断，其特征在于低水平的V γ 3 TCR和高水平的热稳定抗原。这些结果表明，p56 lck和CD 45都参与了胎儿胸腺中V γ 3 T细胞成熟过程中的信号转导。
To determine whether p56lck protein tyrosine kinase and CD45 protein tyrosine phosphatase are involved in the signal transduction during intrathymic differentiation of gamma/delta T cells, we have examined the development of T cells expressing V gamma 3 T cell receptor (TCR) in mice deficient for either protein. The skin from both mice contained significantly reduced numbers of dendritic epidermal T cells expressing decreased levels of V gamma 3 TCR at the cell surface. Analysis of the fetal thymus from these mice suggested that maturation of V gamma 3 thymocytes was blocked at the immature stage that was characterized by the low level of V gamma 3 TCR and the high level of heat stable antigen. These results imply that both p56lck and CD45 are involved in the signal transduction during maturation of V gamma 3 T cells in the fetal thymus.