1. Activated IL-22 pathway occurs in the muscle tissues of patients with polymyositis or dermatomyositis and is correlated with disease activity.
- Author
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Ciccia F, Rizzo A, Alessandro R, Guggino G, Maugeri R, Saieva L, Cannizzaro A, Giardina A, De Leo G, Gerardo Iacopino D, and Triolo G
- Subjects
- Biopsy, Case-Control Studies, Dermatomyositis pathology, Dermatomyositis physiopathology, Humans, Inflammation metabolism, Inflammation pathology, Inflammation physiopathology, Muscle, Skeletal pathology, Muscle, Skeletal physiopathology, Necrosis metabolism, Necrosis pathology, Necrosis physiopathology, Polymyositis pathology, Polymyositis physiopathology, RNA, Messenger metabolism, Receptors, Interleukin metabolism, STAT3 Transcription Factor metabolism, Interleukin-22, Dermatomyositis metabolism, Interleukins metabolism, Muscle, Skeletal metabolism, Polymyositis metabolism, Severity of Illness Index, Signal Transduction physiology
- Abstract
Objective: The aim of this study was to assess the expression of IL-22, IL-22 receptor 1 (IL-22R1), IL-22 binding protein (IL-22BP) and p-STAT3 in muscle tissue from patients with PM and DM., Methods: Levels of IL-22, IL-22R1, IL-22BP and STAT3 mRNA were quantified by RT-PCR. The expression of IL-22, IL-22R1, IL-22BP and p-STAT3 was also analysed using immunohistochemistry., Results: Significant modulation of the IL-22 pathway was observed in inflammatory myopathic tissues. In particular, a significant overexpression of IL-22 at the protein but not the mRNA level was observed in PM/DM tissues and was correlated with myositis activity. IL-22R1 aberrant expression was also observed among infiltrating mononuclear cells and necrotic muscle cells. IL-22BP, which inhibits IL-22 signalling, was expressed only in some muscle fibres in PM/DM patients., Conclusion: Our findings indicate that the IL-22 pathway is activated in inflammatory myopathic tissues and may be involved in the induction of muscle inflammatory processes and muscle necrosis., (© The Author 2014. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)
- Published
- 2014
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