The role of the sympathetic neuroimmune modulation of the B cell in arthritis

B 细胞交感神经免疫调节在关节炎中的作用

• 批准号: 163619631
• 负责人: Professor Dr. Georg Pongratz
• 金额: --
• 依托单位: Krankenhaus Barmherzige Brüder Regensburg
• 依托单位国家: 德国
• 项目类别: Research Units
• 财政年份: 2010
• 资助国家: 德国
• 起止时间: 2009-12-31 至 2013-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/163619631?language=en
• 关键词: role; sympathetic; neuroimmune; modulation; cell

Rheumatoid arthritis (RA) is the most common rheumatic disease and affects 1% of the population. Recent studies have shown that the sympathetic nervous system (SNS) by release of sympathetic neurotransmitters and subsequent stimulation of receptors on immune cells has a profound effect on the course and development of arthritis. One of those immune cells that is susceptible for signals from the sympathetic nervous system, is the B cell, which has been shown to increase antibody production following stimulation with the sympathetic neurotransmitter norepinephrine in own recent work. On the other hand, B cells also contribute to the pathogenesis of arthritis by several means (antigen presentation, cytokine production, and autoantibody secretion). However, the role of sympathetic neuroimmunomodulation of B cells and its effect on the development and severity of arthritis is not known and will be investigated in this project using isolated human synovial B cells, as well as utilizing an established model of collagen-type II induced arthritis. This project will delineate new possible therapeutic targets at the interface between the SNS and the B cell in arthritis.

风湿性关节炎（RA）是最常见的风湿性疾病，影响1%的人口。最近的研究表明，交感神经系统（SNS）通过释放交感神经递质和随后刺激免疫细胞上的受体，对关节炎的病程和发展有深远的影响。对来自交感神经系统的信号敏感的那些免疫细胞之一是B细胞，其在自己最近的工作中已经显示出在用交感神经递质去甲肾上腺素刺激后增加抗体产生。另一方面，B细胞也通过几种方式（抗原呈递、细胞因子产生和自身抗体分泌）参与关节炎的发病机制。然而，B细胞的交感神经免疫调节的作用及其对关节炎的发展和严重程度的影响尚不清楚，将在本项目中使用分离的人滑膜B细胞以及利用已建立的II型胶原诱导的关节炎模型进行研究。该项目将在关节炎中SNS和B细胞之间的界面描绘新的可能的治疗靶点。