Increased expression of PI-3K in asthmatic rat T lymphocytes

被引：0

作者：

Jin Liu

Shixin Zhou

Shengdao Xiong

Yongjian Xu

Zhenxiang Zhang

Weining Xiong

机构：

[1] Huazhong University of Science and Technology,Department of Respiratory Medicine, Tongji Hospital, Tongji Medical College

来源：

Journal of Huazhong University of Science and Technology | 2007年 / 27卷

关键词：

PI-3K; asthma; T helper 2 cell; interleukin-4;

D O I：

暂无

中图分类号：

学科分类号：

摘要：

In order to explore the expression of PI-3K in T lymphocytes of asthmatic rats and the relationship between PI-3K and activation of T lymphocytes, 24 Wistar rats were randomly divided into 4 groups: normal control group, asthmatic one-week group, asthmatic two-week group and asthmatic four-week group. T cells were purified from blood of each rat and the expression of PI-3K was observed by immunocytochemical fluorescence staining, the semiquantitative fluorescence intensity was measured by HPIAS-2000 analytic software, and the expression of IL-4 in supernatants was detected by ELISA. The results showed that the fluorescence intensity of T lymphocytes in asthmatic groups was significantly higher than that in normal control (P<0.001), indicating that the expression of PI-3K in T lymphocytes of asthmatic rats was significantly higher than that in those of normal controls, and the difference between acute and chronic stage asthmatic groups was significant (P<0.05). The expression levels of IL-4 protein in supernatants of asthmatic T lymphocytes were significantly higher than those in the normal controls (P<0.05). There was a significant positive correlation between the expression of PI-3K in T lymphocytes and the IL-4 protein expression in supernatants (r=0.583, P<0.01). It was suggested that PI-3K signal pathway may participate in the processes of activation and other cytological effects of asthmatic T lymphocytes, thus may play an important roles in the pathogenesis of asthma.

引用

页码：34 / 36

页数：2

共 32 条

[1]

Appleman L. J.(2002)CD28 costimulation mediates down-regulation of p27kipl and cell cycle progression by activation of the PI3K/PKB signaling pathway in primary human T cells J Immunol 168 2729-2736

[2]

van Puijenbroek A. A.(2004)CD152 (CTLA-4) determines the unequal resistance of Th1 and Th2 cells against activation-induced cell death by a mechanism requiring PI3 kinase function J Exp Med 199 831-842

[3]

Shu K. M.(2003)Blockade of inflammation and airway hyperresponsiveness in immune-sensitized mice by dominant-negative phosphoinositide 3-Kinase-TAT J Exp Med 198 1573-1582

[4]

Pandiyan P.(2003)Signal transduction mechanism of PKC in the proliferation course of asthmatic rat bronchial smooth muscle cells Chin J Tuberc Respir Dis (Chinese) 26 756-760

[5]

Gärtner D.(2001)The role of nuclear factor-κB and protain kinase C in the signal pathway regulating the expression of Th2 cytokines in asthma Chin J Tuberc Respir Dis (Chinese) 24 355-359

[6]

Soezeri O.(2005)Inhibitors of mitogen-activated protein kinases differentially regulate costimulated T cell cytokine production and mouse airway eosinophilia Respir Res 6 36-330

[7]

Myou S.(2003)PI3K in lymphocyte development, differentiation and activation Nat Rev Immunol 3 317-335

[8]

Leff A. R.(2004)Phosphoinositide 3-kinase in T cell activation and survival Biochem Soc Trans 32 332-5805

[9]

Myo S.(2001)Myb transcription is activated by protein kinase B (PKB) following interleukin-2 stimulation of T cells and is required for PKB mediated protection from apoptosis Mol Cell Biol 21 5797-33 767

[10]

Xu S. Y.(2004)Involvement of 3-phosphoinositide-dependent protein kinase-1 in the MEK/MAPK signal transduction pathway J Biol Chem 279 33 759-F938

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