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通过sCD39/Anti-CD3治疗扭转实验性自身免疫糖尿病的情况

Carmen Fotino¹, R Damaris Molano¹, Moufida Ben Nasr^2,3

¹Cell Transplant Center, Diabetes Research Institute, University of Miami, Miami, FL.

|August 25, 2023

概括

通过可溶性CD39 (sCD39) 向细胞外ATP (eATP) 降解,显示出治疗自身免疫性糖尿病的前景. 这种方法降低了eATP,抑制了T细胞增殖,并延迟了NOD小鼠的1型糖尿病发病.

科学领域:

免疫学免疫学免疫学
内分泌学在内分泌学.
分子生物学分子生物学

背景情况:

细胞外ATP (eATP) 是受损细胞释放的促炎媒介.
CD39和CD73是降解eATP的膜核酸酶.
在自身免疫性糖尿病中eATP降解的作用仍然在很大程度上未被探索.

研究的目的:

研究eATP降解在自身免疫性糖尿病中的作用.
在1型糖尿病 (T1D) 的小鼠模型中评估可溶性CD39 (sCD39) 的治疗潜力.

主要方法:

测量NOD小鼠在不同疾病阶段的eATP水平.
对免疫细胞和胰腺细胞的CD39和CD73表达的评估.
在NOD小鼠的预防和逆转研究中给予sCD39.
评估T细胞增殖,调控T细胞频率和血糖控制.

主要成果:

与糖尿病前的小鼠相比,高血糖NOD小鼠表现出较高的eATP水平.
CD39和CD73在胰腺细胞和T细胞上表达.
sCD39的使用降低了eATP,抑制了自身反应性T细胞的增殖,并增加了调节性T细胞.
sCD39延迟了T1D发病,并与抗CD3疗法在恢复正常血糖症方面表现出协同效应.

结论:

eATP/CD39通路在T1D的病原发生过程中至关重要.
针对eATP降解是T1D的潜在治疗策略.

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