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在多发性硬化症中,循环溶性CD226的水平增加

Saniya Kari¹, Florence Bucciarelli¹, Thibault Angles¹

¹Toulouse Institute for Infectious and Inflammatory Diseases (INFINITY), INSERM UMR1291, CNRS UMR5051, Université Toulouse III, Toulouse Cedex 3, France.

Multiple sclerosis (Houndmills, Basingstoke, England)

|March 1, 2024

概括

可溶性CD226 (sCD226) 在多发性硬化症 (MS) 和光学神经炎 (NMO) 中升高,这表明T细胞激活释放sCD226,可能促进神经炎症.

科学领域:

免疫学免疫学免疫学
神经科学是一个神经科学.
生物化学生物化学

背景情况:

糖蛋白CD226对于免疫细胞调节至关重要.
可溶性CD226 (sCD226) 在慢性炎症疾病中升高.
在多发性硬化症 (MS) 等神经炎症疾病中的sCD226水平仍然未知.

研究的目的:

研究sCD226在患有多发性硬化症 (pwMS) 和其他神经疾病的人群中的存在和功能作用.
确定sCD226是否是神经炎症的潜在生物标志物.

主要方法:

分析了CD226表面表达和T细胞超级生物,以了解sCD226的生产机制.
评估了sCD226对树突细胞成熟的影响.
在健康捐赠者 (HD),pwMS,光学神经炎 (NMO) 和阿尔茨海默病 (AD) 患者中测量了sCD226血清度.

主要成果:

用CD3/CD226诱导的CD226脱落进行T细胞共刺激,释放sCD226.
sCD226添加到成熟的树突细胞增加了促炎性互白素-23 (IL-23) 的产生.
与HD和AD患者相比,pwMS和NMO患者发现sCD226水平明显升高.
多发性硬化症患者,包括复发性缓解性多发性硬化症 (RRMS) 和二次进展性多发性硬化症 (SPMS),与临床隔离综合征 (CIS) 相比,sCD226增加.

结论:

T细胞激活释放sCD226,这可能导致神经炎症.
sCD226有可能成为MS等神经炎症疾病的生物标志物.

关键词:

CD4+ T 细胞是 CD4+ T 细胞.多发性硬化症是多发性硬化症.生物标志物生物标志物树突细胞是一种树突细胞.可溶性CD226是可以溶解的CD226

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