Activation of innate immunity has been linked to the progression of type 1 diabetes. A study now shows that overexpression of METTL3, a writer protein of the m6A machinery that modifies mRNA, restrains interferon-stimulated genes when expressed in pancreatic β-cells, identifying it as a promising therapeutic target.

中文翻译：

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METTL3 抑制 β 细胞的自身免疫

先天免疫的激活与 1 型糖尿病的进展有关。现在的一项研究表明，METTL3（一种修饰 mRNA 的 m6A 机制的写入蛋白）的过度表达，在胰腺 β 细胞中表达时抑制干扰素刺激的基因，从而将其确定为有希望的治疗靶点。