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IFN-β-specific signaling via a unique IFNAR1 interaction

机译：通过独特的IFNAR1相互作用产生IFN-β特异性信号

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The family of type I interferons includes I several members, all of which exhibit important antiviral, antineoplastic and immu-nomodulary properties in vitro and in vivo. Members of this family include the various intcrferon-a (IFN-alpha) subtypes, as well as IFN-beta, IFN-alpha), IFN-T, IFN-k and IFN-e. Although all type I interferons bind to the same receptor, the type I interferon receptor (IFNR), and activate a common set of signaling elements, there is evidence for specific responses by IFN-beta and differences between IFN-β and other type I interferons in their biological outcomes. Despite extensive work by many groups in this research area, the mechanisms by which such IFN-beta specificity is defined have remained largely unknown. In this issue of Nature Immunology, de Weerd et at provide evidence for a unique and specific complex formed between IFN-beta and IFNAR1, one of the subunits of the type I IFNR. Although such interaction is not sufficient to ignite activation of classical signaling via Jak kinases and STAT transcription factors, it is sufficient to generate signals that control the transcription of a unique group of genes that do not require activation of STAT1 for their expression. This surprising discovery is important and has substantial biological and, possibly, clinical-translational implications.
机译：I型干扰素家族包括几个成员，它们在体外和体内均表现出重要的抗病毒，抗肿瘤和免疫调节特性。该家族的成员包括各种干扰素-α（IFN-α）亚型，以及IFN-β，IFN-α，IFN-T，IFN-k和IFN-e。尽管所有I型干扰素都与相同的受体I型干扰素受体（IFNR）结合并激活一组共同的信号传导元件，但有证据表明IFN-β会产生特异性反应以及IFN-β与其他I型干扰素之间的差异他们的生物学结果。尽管该研究领域的许多研究小组进行了大量工作，但定义这种IFN-β特异性的机制仍在很大程度上未知。在本期《自然免疫学》中，de Weerd等人提供了证据，证明了IFN-β和IFNAR1（I型IFNR的亚基之一）之间形成了独特而特殊的复合物。尽管这种相互作用不足以激发通过Jak激酶和STAT转录因子激活经典信号传导，但足以生成控制一组独特基因转录的信号，这些基因不需要激活STAT1即可表达。这一令人惊讶的发现很重要，并且具有重要的生物学和可能的临床翻译意义。

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