Maneechotesuwan Kittipong, Xin Yao, Ito Kazuhiro, Jazrawi Elen, Lee Kang-Yun, Usmani Omar S, Barnes Peter J, Adcock Ian M
Section of Airway Disease, National Heart and Lung Institute, Imperial College, London, United Kingdom.
J Immunol. 2007 Feb 15;178(4):2491-8. doi: 10.4049/jimmunol.178.4.2491.
GATA-3 plays a critical role in allergic diseases by regulating the release of cytokines from Th2 lymphocytes. However, the molecular mechanisms involved in the regulation of GATA-3 in human T lymphocytes are not yet understood. Using small interfering RNA to knock down GATA-3, we have demonstrated its critical role in regulating IL-4, IL-5, and IL-13 release from a human T cell line. Specific stimulation of T lymphocytes by costimulation of CD3 and CD28 to mimic activation by APCs induces translocation of GATA-3 from the cytoplasm to the nucleus, with binding to the promoter region of Th2 cytokine genes, as determined by chromatin immunoprecipitation. GATA-3 nuclear translocation is dependent on its phosphorylation on serine residues by p38 MAPK, which facilitates interaction with the nuclear transporter protein importin-alpha. This provides a means whereby allergen exposure leads to the expression of Th2 cytokines, and this novel mechanism may provide new approaches to treating allergic diseases.
GATA-3通过调节Th2淋巴细胞释放细胞因子,在过敏性疾病中发挥关键作用。然而,人类T淋巴细胞中GATA-3调节的分子机制尚不清楚。利用小干扰RNA敲低GATA-3,我们已证明其在调节人T细胞系释放IL-4、IL-5和IL-13中的关键作用。通过共刺激CD3和CD28特异性刺激T淋巴细胞以模拟抗原呈递细胞的激活,可诱导GATA-3从细胞质转位至细胞核,并与Th2细胞因子基因的启动子区域结合,这是通过染色质免疫沉淀确定的。GATA-3核转位依赖于p38丝裂原活化蛋白激酶对其丝氨酸残基的磷酸化作用,这促进了与核转运蛋白输入蛋白α的相互作用。这提供了一种过敏原暴露导致Th2细胞因子表达的途径,这种新机制可能为治疗过敏性疾病提供新方法。