Role of non-immune mechanisms of muscle damage in idiopathic inflammatory myopathies.
Role of non-immune mechanisms of muscle damage in idiopathic inflammatory myopathies.
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DOI：
10.1186/ar3791
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发表时间：
2012-04-27
影响因子：
4.9
通讯作者：
Nagaraju K
中科院分区：
文献类型：
--
作者：
Coley W;Rayavarapu S;Nagaraju K
特发性炎症性肌病（IIMs）包括一组自身免疫性疾病，其特征是对称性骨骼肌无力和肌肉炎症，原因不明。像其他自身免疫性疾病一样，IIMs可以用糖皮质激素或免疫抑制药物治疗。然而，许多IIM患者经常对免疫抑制治疗产生耐药性，并且有令人信服的证据表明，不仅适应性免疫机制，而且几种非免疫机制在这些疾病的发病机制中起作用。在这里，我们关注一些与病理机制相关的证据，如先天免疫反应、内质网应激、MHC I类过表达的非免疫后果、代谢紊乱和缺氧。这些机制可以解释iim相关的病理过程如何在面对免疫抑制治疗时仍能继续。这些数据表明，IIMs的治疗策略应针对肌肉损伤的免疫和非免疫机制。
Idiopathic inflammatory myopathies (IIMs) comprise a group of autoimmune diseases that are characterized by symmetrical skeletal muscle weakness and muscle inflammation with no known cause. Like other autoimmune diseases, IIMs are treated with either glucocorticoids or immunosuppressive drugs. However, many patients with an IIM are frequently resistant to immunosuppressive treatments, and there is compelling evidence to indicate that not only adaptive immune but also several non-immune mechanisms play a role in the pathogenesis of these disorders. Here, we focus on some of the evidence related to pathologic mechanisms, such as the innate immune response, endoplasmic reticulum stress, non-immune consequences of MHC class I overexpression, metabolic disturbances, and hypoxia. These mechanisms may explain how IIM-related pathologic processes can continue even in the face of immunosuppressive therapies. These data indicate that therapeutic strategies in IIMs should be directed at both immune and non-immune mechanisms of muscle damage.
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DOI：
10.1083/jcb.200303157
发表时间：
2003-08-04
期刊：
The Journal of cell biology
影响因子：
--
作者：
Kalai M;Lamkanfi M;Denecker G;Boogmans M;Lippens S;Meeus A;Declercq W;Vandenabeele P
通讯作者：
Vandenabeele P
组酰基TRNA合成酶和天冬酰基-TRNA合成酶，肌炎中的自身抗原，激活T淋巴细胞上的趋化因子受体和未成熟的树突状细胞。
影响因子：
15.3
作者：
Howard, O M Zack;Dong, Hui Fang;Yang, De;Raben, Nina;Nagaraju, Kanneboyina;Rosen, Antony;Casciola-Rosen, Livia;Hartlein, Michael;Kron, Michael;Yang, David;Yiadom, Kwabena;Dwivedi, Sunita;Plotz, Paul H;Oppenheim, Joost J
通讯作者：
Oppenheim, Joost J
影响因子：
27.4
作者：
Brouwer, R;Hengstman, GJD;van Venrooij, WJ
通讯作者：
van Venrooij, WJ
影响因子：
15.9
作者：
Goebels, N;Michaelis, D;Hohlfeld, R
通讯作者：
Hohlfeld, R
影响因子：
6
作者：
Fratta, P;Engel, WK;Askanas, V
通讯作者：
Askanas, V