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抑制TH17分化和自身免疫通过合成ROR连接体抑制TH17分化和自身免疫
Laura A Solt1, Naresh Kumar, Philippe Nuhant
1Department of Molecular Therapeutics, The Scripps Research Institute, Jupiter, Florida 33458, USA.
Nature
|April 19, 2011
概括
一种新的化合物SR1001专门针对RORα和RORγt核受体. 这种抑制有效地抑制了T(H) 17细胞的分化和功能,为自身免疫性疾病的治疗提供了潜力.
科学领域:
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
- 药理学 药理学 是一个学科.
背景情况:
- 辅助T细胞17 (T(H) 17是CD4(+) T细胞,与自身免疫性疾病有关.
- RORα和RORγt核受体对于T(H) 17细胞发育至关重要.
研究的目的:
- 开发一种针对RORα和RORγt的新型化合物.
- 为了研究这种化合物在抑制T(H) 17细胞分化和功能的有效性.
- 评估自身免疫性疾病模型中的治疗潜力.
主要方法:
- 开发了SR1001,一种特定的双重RORα/RORγt连接体.
- 评估了SR1001对RORα/RORγt的结合和构成作用.
- 评估了SR1001对小鼠T(H) 17细胞发育和细胞因子产生的影响.
- 在自身免疫疾病的小鼠模型中测试了SR1001.
主要成果:
- SR1001特别结合RORα和RORγt,改变受体构造和转录活性.
- SR1001在发育中的T(H) 17细胞中抑制了介素-17A基因和蛋白质的表达.
- 在分化的人类和小鼠T (H) 17细胞中,SR1001抑制了细胞因子的产生.
- 在小鼠中,SR1001治疗显著降低了自身免疫性疾病的临床严重程度.
结论:
- 用SR1001向RORα和RORγt,特别抑制T(H) 17细胞的分化和功能.
- SR1001代表了一种新的化合物类别,具有治疗自身免疫性疾病的潜力.
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