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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >The p110gamma isoform of phosphatidylinositol 3-kinase regulates migration of effector CD4 T lymphocytes into peripheral inflammatory sites.
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The p110gamma isoform of phosphatidylinositol 3-kinase regulates migration of effector CD4 T lymphocytes into peripheral inflammatory sites.

机译：磷脂酰肌醇3-激酶的p110γ亚型可调节效应CD4 T淋巴细胞向周围炎症部位的迁移。

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摘要

The role of PI-3K in leukocyte function has been studied extensively. However, the specific role of the p110gamma isoform of PI- 3K in CD4 T lymphocyte function has yet to be defined explicitly. In this study, we report that although p110gamma does not regulate antigen-dependent CD4 T cell activation and proliferation, it plays a crucial role in regulating CD4 effector T cell migration. Naive p110gamma(-/-) CD4 lymphocytes are phenotypically identical to their wild-type (WT) counterparts and do not exhibit any defects in TCR-mediated calcium mobilization or Erk activation. In addition, p110gamma-deficient CD4 OT.II T cells become activated and proliferate comparably with WT cells in response to antigen in vivo. Interestingly, however, antigen-experienced, p110gamma-deficient CD4 OT.II lymphocytes exhibit dramatic defects in their ability to traffic to peripheral inflammatory sites in vivo. Although antigen-activated, p110gamma-deficient CD4 T cells express P-selectin ligand, beta2 integrin, beta1 integrin, CCR4, CXCR5, and CCR7 comparably with WT cells, they exhibit impaired F-actin polarization and migration in response to stimulation ex vivo with the CCR4 ligand CCL22. These findings suggest that p110gamma regulates the migration of antigen-experienced effector CD4 T lymphocytes into inflammatory sites during adaptive immune responses in vivo.
机译：PI-3K在白细胞功能中的作用已被广泛研究。但是，PI-3K的p110gamma亚型在CD4 T淋巴细胞功能中的特定作用尚未明确定义。在这项研究中，我们报告，尽管p110gamma不能调节抗原依赖性CD4 T细胞的活化和增殖，但在调节CD4效应T细胞迁移中起着至关重要的作用。幼稚的p110gamma（-/-）CD4淋巴细胞在表型上与其野生型（WT）对应物相同，并且在TCR介导的钙动员或Erk激活中没有任何缺陷。另外，p110γ-缺陷的CD4 OT.II T细胞在体内对抗原的应答中被激活并与WT细胞相比增殖。然而，有趣的是，经历过抗原，p110γ缺陷的CD4 OT.II淋巴细胞在体内向周围炎症部位的运输能力上显示出明显的缺陷。尽管抗原激活的p110γ缺陷型CD4 T细胞与WT细胞表达P-选择蛋白配体，β2整联蛋白，β1整联蛋白，CCR4，CXCR5和CCR7相比，但它们表现出受损的F-肌动蛋白极化和迁移，这是由于体外刺激CCR4配体CCL22。这些发现表明，在体内适应性免疫应答过程中，p110γ调节抗原经历的效应器CD4 T淋巴细胞向炎症位点的迁移。

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