<br>I、II 和 III 型干扰素在肌炎中的作用：综述,Brain Pathology

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I、II 和 III 型干扰素在肌炎中的作用：综述
Brain Pathology ( IF 5.8 ) Pub Date : 2021-05-27 , DOI: 10.1111/bpa.12955
Loïs Bolko ₁ , Wei Jiang _{2,

3} , Nozomu Tawara _{2,

3} , Océane Landon-Cardinal _{4,

5} , Céline Anquetil _{2,

3} , Olivier Benveniste _{2,

3} , Yves Allenbach _{2,

3}

Affiliation

特发性炎症性肌病 (IIM) 的分类基于临床、血清学和组织学标准。肌炎特异性抗体的鉴定有助于将更同质的肌炎群体定义为四个主要亚型：皮肌炎（DM）、抗合成酶综合征（ASyS）、散发性包涵体肌炎（sIBM）和免疫介导的坏死性肌病（IMNM）。 sIBM 和 IMNM 患者主要表现为肌肉受累，而 DM 和 ASyS 患者还表现为其他肌肉外特征，如皮肤、肺和关节表现。此外，每个肌炎亚型之间的病理生理机制是不同的。最近，干扰素（IFN）途径已被确定为参与肌炎病理生理学的关键参与者。在 DM 中，IFN（尤其是 I 型 IFN）的关键作用得到了 DM 患者肌肉、血液和皮肤中 IFN 特征的鉴定的支持。此外，DM 特异性抗体靶向参与 IFN 信号通路的抗原。 I 型干扰素的致病性已通过导致遗传性疾病（单基因干扰素病）的干扰素途径突变的鉴定得到证实。 IFN 信号通路的这种组成性激活可诱发全身性表现，如间质性肺病、肌炎和皮疹。由于 DM 患者在 IFN 信号通路获得性激活方面具有相似的特征，因此我们可以将单基因疾病的基本概念扩展到获得性干扰素病，例如 DM。相反，在 ASyS 中，现有数据表明 II 型 IFN 在血液、肌肉和肺中发挥作用。事实上，转录组分析强调了 ASyS 肌肉组织中 II 型 IFN 基因的表达。在 sIBM 中，II 型 IFN 似乎是参与肌肉炎症机制的重要细胞因子，并可能与肌退行性特征相关。对于 IMNM，目前发表的数据很少，表明 II 型 IFN 的影响较小。本综述强调了不同干扰素亚型及其在每个肌炎亚型中的具体分子机制。

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The role of interferons type I, II and III in myositis: A review

The classification of idiopathic inflammatory myopathies (IIM) is based on clinical, serological and histological criteria. The identification of myositis-specific antibodies has helped to define more homogeneous groups of myositis into four dominant subsets: dermatomyositis (DM), antisynthetase syndrome (ASyS), sporadic inclusion body myositis (sIBM) and immune-mediated necrotising myopathy (IMNM). sIBM and IMNM patients present predominantly with muscle involvement, whereas DM and ASyS patients present additionally with other extramuscular features, such as skin, lung and joints manifestations. Moreover, the pathophysiological mechanisms are distinct between each myositis subsets. Recently, interferon (IFN) pathways have been identified as key players implicated in the pathophysiology of myositis. In DM, the key role of IFN, especially type I IFN, has been supported by the identification of an IFN signature in muscle, blood and skin of DM patients. In addition, DM-specific antibodies are targeting antigens involved in the IFN signalling pathways. The pathogenicity of type I IFN has been demonstrated by the identification of mutations in the IFN pathways leading to genetic diseases, the monogenic interferonopathies. This constitutive activation of IFN signalling pathways induces systemic manifestations such as interstitial lung disease, myositis and skin rashes. Since DM patients share similar features in the context of an acquired activation of the IFN signalling pathways, we may extend underlying concepts of monogenic diseases to acquired interferonopathy such as DM. Conversely, in ASyS, available data suggest a role of type II IFN in blood, muscle and lung. Indeed, transcriptomic analyses highlighted a type II IFN gene expression in ASyS muscle tissue. In sIBM, type II IFN appears to be an important cytokine involved in muscle inflammation mechanisms and potentially linked to myodegenerative features. For IMNM, currently published data are scarce, suggesting a minor implication of type II IFN. This review highlights the involvement of different IFN subtypes and their specific molecular mechanisms in each myositis subset.

更新日期：2021-05-27

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