Abstract
Recent studies suggest a mechanistic role for molecules induced by type 1 interferons in the pathogenesis of some forms of myositis. For dermatomyositis, evidence that these molecules injure myofibers seems especially strong. In the group of disorders known as polymyositis, the study of blood samples suggests a potential role. It is unknown what drives the sustained presence of type 1 interferon-inducible molecules in these diseases, as the type 1 interferons themselves have not been specifically detected along with their downstream biomarkers. Therapeutic development for blockade of IFNα is in progress aided by the identification of blood genomic biomarkers.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Biomarkers
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Dermatomyositis / blood
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Dermatomyositis / diagnosis
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Dermatomyositis / etiology
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Dermatomyositis / immunology
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Dermatomyositis / pathology
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Diagnosis, Differential
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Gene Expression Regulation / immunology
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Humans
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Interferon Type I / antagonists & inhibitors
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Interferon Type I / biosynthesis
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Interferon Type I / blood
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Interferon Type I / genetics
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Interferon Type I / immunology*
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Molecular Targeted Therapy
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Muscle, Skeletal / blood supply
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Muscle, Skeletal / immunology
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Muscle, Skeletal / pathology
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Myositis, Inclusion Body / blood
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Myositis, Inclusion Body / diagnosis
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Myositis, Inclusion Body / etiology
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Myositis, Inclusion Body / immunology
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Myositis, Inclusion Body / pathology
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Organ Specificity
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Polymyositis / blood
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Polymyositis / etiology*
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Polymyositis / immunology
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Polymyositis / pathology
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RNA, Messenger / biosynthesis
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RNA, Messenger / blood
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Receptor, Interferon alpha-beta / antagonists & inhibitors
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Receptor, Interferon alpha-beta / physiology
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Signal Transduction
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Skin / immunology
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Skin / pathology
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Transcription, Genetic
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Tumor Necrosis Factor-alpha / physiology
Substances
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Biomarkers
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IFNAR1 protein, human
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Interferon Type I
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RNA, Messenger
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Tumor Necrosis Factor-alpha
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Receptor, Interferon alpha-beta