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Review
. 2012 Apr 27;14(2):209.
doi: 10.1186/ar3791.

Role of non-immune mechanisms of muscle damage in idiopathic inflammatory myopathies

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Review

Role of non-immune mechanisms of muscle damage in idiopathic inflammatory myopathies

William Coley et al. Arthritis Res Ther. .

Abstract

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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Figures

Figure 1
Figure 1
Relationship between the possible pathologic mechanisms leading to idiopathic inflammatory myopathies.ER, endoplasmic reticulum; MHC, major histocompatibility complex; TLR, Toll-like receptor.

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References

    1. Mastaglia FL, Garlepp MJ, Phillips BA, Zilko PJ. Inflammatory myopathies: clinical, diagnostic and therapeutic aspects. Muscle Nerve. 2003;27:407–425. doi: 10.1002/mus.10313. - DOI - PubMed
    1. Tanimoto K, Nakano K, Kano S, Mori S, Ueki H, Nishitani H, Sato T, Kiuchi T, Ohashi Y. Classification criteria for polymyositis and dermatomyositis. J Rheumatol. 1995;22:668–674. - PubMed
    1. Miller F, Rider L, Plotz P, Oddis C, Isenberg D. Diagnostic criteria for polymyositis and dermatomyositis. Lancet. 2003;362:1762–1763. doi: 10.1016/S0140-6736(03)14862-3. - DOI - PubMed
    1. Santmyire-Rosenberger B, Dugan EM. Skin involvement in dermatomyositis. Curr Opin Rheumatol. 2003;15:714–722. doi: 10.1097/00002281-200311000-00006. - DOI - PubMed
    1. Ramanan AV, Feldman BM. Clinical features and outcomes of juvenile dermatomyositis and other childhood onset myositis syndromes. Rheum Dis Clin North Am. 2002;28:833–857. doi: 10.1016/S0889-857X(02)00024-8. - DOI - PubMed

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