Phosphoinositide 3-Kinase p1101γ in Immunity

被引:31
作者
Costa, Carlotta [1 ,2 ]
Martin-Conte, Erica L. [3 ]
Hirsch, Emilio [1 ,2 ]
机构
[1] Univ Turin, Dept Genet Biol & Biochem, I-10126 Turin, Italy
[2] Univ Turin, Ctr Mol Biotechnol, I-10126 Turin, Italy
[3] Univ Turin, Dept Anesthesiol & Crit Care, Osped S Giovanni Battista Molinette, I-10126 Turin, Italy
关键词
phospholipid signaling; PI3-kinase; T-CELL-ACTIVATION; INDUCED LUNG INJURY; MAST-CELLS; PHOSPHATIDYLINOSITOL; 3-KINASE-GAMMA; PULMONARY INFLAMMATION; RHEUMATOID-ARTHRITIS; MACROPHAGE-MIGRATION; IN-VIVO; PI3K-GAMMA; GAMMA;
D O I
10.1002/iub.516
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The rapid and accurate response of leukocytes to environmental cues is critical for a proper inflammatory reaction to foreign particles or invading microbes. In the last decade, the signal transduction enzyme phosphoinositide 3-kinase gamma (PI3K gamma) has emerged as a critical modulator of leukocyte responses, with its effects spanning from recruitment to the site of inflammation to the production of reactive oxygen species. These findings initially obtained from genetically modified mice have led to the development of experimental anti-inflammatory inhibitors with reasonable selectivity and specificity. While such molecules have not yet reached clinical use, preclinical studies combining genetics and pharmacology continue to provide new therapeutic indications for targeting PI3K gamma. Thus, this review focuses on the latest discoveries regarding PI3K gamma function in leukocytes and on the most recent findings in disease models related to immunity. (C) 2011 IUBMB IUBMB Life, 63(9): 707-713, 2011
引用
收藏
页码:707 / 713
页数:7
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