盖莱克-3调解NETosis,并在系统性狼红斑相关的扩散气膜出血中充当自身抗原
Shih-Yao Chen1, Chung-Teng Wang2,3, Ching-Yi Chen4
1Department of Nursing, College of Nursing, Chung Hwa University of Medical Technology, Tainan 71703, Taiwan.
International journal of molecular sciences
|June 10, 2023
概括
在全身性红斑狼 (SLE) 患者中,加列-3的水平升高,并驱动 NETosis,这是疾病的关键因素. 减少galectin-3提高了生存率,并减少了小鼠的狼症状,这表明它是一个治疗目标.
科学领域:
- 免疫学 免疫学 免疫学
- 类风湿病学 类风湿病学
- 分子生物学分子生物学
背景情况:
- 系统性红斑狼 (SLE) 是一种自身免疫性疾病,其特征是增强的NETosis和受损的NET退化.
- 加勒-3是一种β-galactoside结合蛋白,涉及中性粒细胞功能和自身免疫性疾病.
研究的目的:
- 调查加勒-3和SLE病原体之间的关联,包括狼性炎 (LN) 和疾病活性.
- 探索加勒-3在NETosis中的作用及其作为SLE治疗点的潜力.
主要方法:
- 从SLE患者的PBMC中量化了galectin-3表达,并将其与LN和SLEDAI-2K相关联.
- 在人类和小鼠中性粒细胞中评估的NETosis,包括加勒-3淘汰赛 (Gal-3 KO) 模型.
- 在Gal-3 KO和野生型 (WT) 小鼠中评估了原始诱导狼的疾病表现.
主要成果:
- 在SLE患者的PBMC中增加的加勒-3水平与LN和SLEDAI-2K正相关.
- 与WT小鼠相比,Gal-3 KO小鼠的生存率提高,DAH,LN,蛋白尿和抗RNP抗体减少.
- 在Gal-3 KO中性粒细胞中观察到降低的NETosis和素基因素3 (CitH3) 水平;在NET中发现了 galectin-3.
结论:
- 盖莱克-3在SLE病变发生过程中起着重要作用,并与疾病的严重程度有关.
- 盖莱克-3促进NETosis,有助于狼的表型.
- 向加列-3为SLE提供了一个有前途的治疗策略.
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