Tec kinase ITK-dependent signaling pathways in the resolution of inflammation in ulcerative colitis (B02)

Tec 激酶 ITK 依赖性信号通路在溃疡性结肠炎炎症消退中的作用 (B02)

• 批准号: 277738419
• 金额: --
• 依托单位: Medizinische Klinik 1 - Gastroenterologie, Pneumologie und Endokrinologie
• 依托单位国家: 德国
• 项目类别: Collaborative Research Centres
• 资助国家: 德国
• 项目状态: 未结题
• 来源: https://gepris.dfg.de/gepris/projekt/277738419?language=en
• 关键词: Tec; kinase; ITK; dependent; signaling

Project B02 (Neurath / Weigmann) is interested in a better mechanistic understanding of the factors that can prevent the resolution of inflammation in the gut. In the last funding period, the crucial role of the Tec kinase ITK in regulating T-cell cytokine responses in ulcerative colitis was uncovered, which prevents the resolution of inflammation. By targeting ITK, both the production of pro-inflammatory cytokines and disease progression could be improved. Based on the preliminary data, which place proteins such as ZAP70, Lck, TIM1 and TIM3 as ITK-interacting modulators at the center of the project, the inflammation-resolving process in the intestine will be investigated in more detail.

项目B 02（Neurath / Weigmann）感兴趣的是更好地了解可以阻止肠道炎症消退的因素的机制。在上一个资助期，Tec激酶ITK在溃疡性结肠炎中调节T细胞细胞因子反应的关键作用被发现，这阻止了炎症的解决。通过靶向ITK，可以改善促炎细胞因子的产生和疾病进展。基于初步数据，将ZAP 70，Lck，TIM 1和TIM 3等蛋白质作为ITK相互作用的调节剂置于该项目的中心，将更详细地研究肠道中的炎症消退过程。