Crosstalk between inflammation, bone destruction and new bone formation in patients with ankylosing spondylitis

炎症和新骨形成是强直性脊柱炎（AS）中观察到的免疫病理学特征，并决定疾病的活动性、功能和长期预后。波动炎症的分子机制及其与新骨形成的相互作用尚不清楚。在目前的项目中，我们将在分子水平上将动物模型中获得的这种相互作用的最新证据应用于从AS患者获得的组织学和免疫组织学骨材料，并辅以体外功能研究。以下问题将被解决：(i) T效应细胞和T调节细胞在炎症中的作用，特别关注TH17细胞；（ii）炎症和新骨形成的细胞和分子之间的相互作用；（iii） AS中与新骨形成相关的细胞/分子的研究。这里获得的结果应该使我们能够开发更好和/或改进当前的治疗方法来抑制AS的炎症和骨增殖。

Inflammation and new bone formation are the hallmarks of the immunopathology observed in ankylosing spondylitis (AS) and determine disease activity, function and longterm outcome. The molecular mechanism of the fluctuating inflammation and its interaction with new bone formation are only poorly understood. In the current project we will apply recent evidence about such an interaction obtained in animal models on the molecular level to histological and immunhistological bone material obtained from AS patients, supplemented by functional in vitro studies. The following question will be addressed: (i) the role of T effector and T regulatory cells in inflammation with special focus on TH17 cells; (ii) interaction between cells and molecules of inflammation and of new bone formation; (iii) investigation of cells/molecules relevant for new bone formation in AS. The results obtained here should enable us to develop better and/or refined current therapies for inhibition of inflammation and osteoproliferaion in AS.