CD22 and its regulation of BCR signaling strength in germinal center B cell fate and metabolism

CD22及其对生发中心B细胞命运和代谢中BCR信号强度的调节

• 批准号: 528069786
• 负责人: Professor Dr. Lars Nitschke
• 金额: --
• 依托单位: Department Biologie
• 依托单位国家: 德国
• 项目类别: Research Units
• 资助国家: 德国
• 项目状态: 未结题
• 来源: https://gepris.dfg.de/gepris/projekt/528069786?language=en
• 关键词: CD22; its; regulation; BCR; signaling

Humoral immune responses are performed by antibodies, which mature in so-called germinal centres, which are specialised structures in spleen and lymph nodes. For this process the signalling response by the B cell receptor (BCR) in germinal center B cells plays an important role. This signalling response is regulated by inhibitory receptors like CD22. In preliminary work we demonstrated that CD22 deficiency causes an enhanced Ca2+ signalling in germinal center B cells. This triggered enhanced apoptosis and a lower number of germinal center B cells, when compared to control animals. In this application it will be studied how enhanced or lower BCR signalling affects B cell fate and metabolism in the germinal center. We will also apply an intravital imaging system in order to be able to follow Ca2+ signalling and metabolism of germinal center B cells in vivo.

体液免疫反应是由抗体完成的，这些抗体在所谓的生发中心（germinal centres）中成熟，生发中心是脾脏和淋巴结中的专门结构。在这一过程中，生殖中心B细胞中的B细胞受体（BCR）的信号应答起着重要作用。这种信号传导反应由抑制性受体如CD22调节。在初步工作中，我们证明，CD 22缺陷导致在生发中心B细胞中Ca2+信号传导增强。与对照动物相比，这引发了增强的凋亡和较低数量的生发中心B细胞。在本申请中，将研究增强或降低的BCR信号传导如何影响B细胞的命运和在生发中心的代谢。我们还将应用活体成像系统，以便能够在体内跟踪生殖中心B细胞的Ca 2+信号传导和代谢。