Nature:RIPK1剪切异常会引起自身炎症性疾病

2019-12-14 海北 MedSci原创

最近,研究人员发现,在人类细胞中,杂合的错义突变D324N,D324H和D324Y可以阻止RIPK1的半胱天冬酶裂解,并导致早发性周期性发热综合征和严重的间歇性淋巴结病,研究人员将这种情况称为“抗裂解性RIPK1诱导的自体炎症综合征”。

RIPK1是先天性免疫信号通路的关键调节因子。为了确保最佳的炎症反应,RIPK1被翻译后修饰所调节,包括已被广泛研究的泛素化和磷酸化事件,以及caspase-8介导的剪切。

尽管人们认为这种剪切事件会抑制RIPK3的激活和坏死,但至今为止,其在生理上的相关性仍不清楚。

最近,研究人员发现,在人类细胞中,杂合的错义突变D324N,D324H和D324Y可以阻止RIPK1的半胱天冬酶裂解,并导致早发性周期性发热综合征和严重的间歇性淋巴结病,研究人员将这种情况称为“抗裂解性RIPK1诱导的自体炎症综合征”。

为了定义这种疾病的机制,研究人员制作了抗裂解的Ripk1D325A突变小鼠品系。 研究人员发现,Ripk1-/-小鼠会死于全身性炎症,而Ripk1D325A / D325A小鼠则在胚胎发生过程中死亡。Casp8和Ripk3的联合缺失可以完全防止胚胎致死,但Ripk3或Mlkl的单独缺失则不能。

RIPK1激酶活性的丧失也阻止了Ripk1D325A / D325A的胚胎致死性,但是这些小鼠在断奶之前会因为依赖RIPK3的方式,发生多器官炎症而死亡。

一致的是,Ripk1D325A / D325A和Ripk1D325A / +的细胞对依赖RIPK3的TNF诱导的细胞凋亡和坏死病敏感。

杂合的Ripk1D325A / +小鼠是可以存活的,并且完全正常,但对体内的炎症刺激会产生过度反应。

因此,这些结果表明,胱天蛋白酶介导的RIPK1剪切在胚胎发育过程中十分重要,RIPK1的胱天蛋白酶的剪切不仅抑制了坏死病,而且在整个生命过程中都保持了炎症稳态。


原始出处:

Najoua Lalaoui et al. Mutations that prevent caspase cleavage of RIPK1 cause autoinflammatory diseaseNature, 2019; DOI: https://doi.org/10.1038/s41586-019-1828-5


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    2020-06-23 huiwelcome
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    2019-12-14 njwbhuang

    新的进展,好文章!

    0