Disruption of epithelial gamma delta T cell repertoires by mutation of the Syk tyrosine kinase
Disruption of epithelial gamma delta T cell repertoires by mutation of the Syk tyrosine kinase
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DOI：
10.1073/pnas.93.18.9704
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发表时间：
1996-09-03
影响因子：
11.1
通讯作者：
Hayday, AC
中科院分区：
文献类型：
--
作者：
MallickWood, CA;Pao, W;Hayday, AC
淋巴细胞缺乏Syk酪氨酸激酶的嵌合小鼠已经被创造出来。与Syk阳性对照相比，Syk- /-淋巴细胞小鼠皮肤和肠道上皮内γ δ T细胞大量耗损，抗原受体基因重排后发生发育停滞。在这种对Syk的依赖性中，上皮内γ δ T细胞亚群与B细胞相似，但与Syk缺陷小鼠中发育和扩增的脾γ δ T细胞不同。某些t细胞受体V γ /V δ基因重排与特定上皮的特征性关联也因Syk缺乏而中断。
Chimeric mice in which lymphocytes are deficient in the Syk tyrosine kinase have been created. Compared with Syk-positive controls, mice with Syk -/- lymphocytes display substantial depletion of intraepithelial gamma delta T cells in the skin and gut, with developmental arrest occurring after antigen receptor gene rearrangement. In this dependence on Syk, subsets of intraepithelial gamma delta T cells are similar to B cells, but distinct from splenic gamma delta T cells that develop and expand in Syk-deficient mice. The characteristic associations of certain T-cell receptor V gamma/V delta gene rearrangements with specific epithelia are also disrupted by Syk deficiency.