J Korean Rheum Assoc.  2008 Jun;15(2):118-122. 10.4078/jkra.2008.15.2.118.

Increased Interleukin-17 Expression in Patients with Idiopathic Inflammatory Myopathies

Affiliations
  • 1Department of Internal Medicine, College of Medicine, Pusan National University, Busan, Korea. ksimd@pusan.ac.kr
  • 2Department of Neurology, College of Medicine, Pusan National University, Busan, Korea.
  • 3Research Institute, College of Medicine, Pusan National University, Busan, Korea.
  • 4Department of Internal Medicine, Busan St. Mary's Medical Center, Busan, Korea.

Abstract

OBJECTIVE: Idiopathic inflammatory myopathies (IIMs) are systemic autoimmune diseases characterized by infiltration of T lymphocytes, monocytes, and macrophages in muscle tissues. Interleukin-17 (IL-17), a Th17 cytokine, has potent pro-inflammatory actions and plays a role in autoimmune diseases. We investigated the expression of IL-17 in muscle tissues of patients with IIMs. METHODS: We measured the IL-17 mRNA level of muscle tissues from 14 patients with IIMs (9 patients with dermatomyositis and 5 patients with polymyositis) by real-time RT-PCR and compared with controls. We also performed an immunohistochemical stain to detect IL-17 expression. RESULTS: The expressions of IL-17 were significantly enhanced in IIMs than controls. In immunohistochemistry, IL-17 was expressed in perimysial, endomysial and perivascular infiltrating inflammatory cells. CONCLUSION: These results suggest that IL-17 plays a role in the immunopathogenesis of IIMs.

Keyword

Interleukin-17; Idiopathic inflammatory myopathies; Dermatomyositis; Polymyositis

Figure

  • Fig. 1. Immunohistochemistry of IL-17 in muscle tissues from patients with IIMs (B, C) and control (A). In DM (B) and PM (C), IL-17 was expressed in perimysial, endomysialand perivascular infiltrating inflammatory cells (arrow). Muscle tissue from control was negative (A). Magnification, ×200. IIMs: idiopathic inflammatory myopathies, DM: dermatomyositis, PM: polymyositis.


Reference

References

1. Briani C, Doria A, Sarzi-Puttini P, Dalakas MC. Update on idiopathic inflammatory myopathies. Autoimmunity. 2006; 39:161–70.
Article
2. Wiendl H, Hoflfeld R, Kieseier BC. Immunobiology of muscle: advances in understanding an immunological microenvironment. Trend Immunol. 2005; 26:373–80.
Article
3. Salomonsson S, Lundberg I. Cytokines in idiopathic inflammatory myopathies. Autoimmunity. 2006; 39:177–90.
Article
4. McFarland HF, Martin R. Multiple sclerosis: a complicated picture of autoimmunity. Nat Immunol. 2007; 8:913–9.
Article
5. Toh ML, Miossec P. The role of T cells in rheumatoid arthritis: new subsets and new targets. Curr Opin Rheumatol. 2007; 19:284–8.
Article
6. Chevrel G, Page G, Granet C, Streichenberger N, Varennes A, Miossec P. Interleukin-17 increases the effects of IL-1 beta on muscle cells: arguments for the role of T cells in the pathogenesis of myositis. J Neuroimmunol. 2003; 137:125–33.
7. Page G, Chevrel G, Miossec P. Anatomic localization of immature and mature dendritic cell subsets in dermatomyositis and polymyositis. Arthritis Rheum. 2004; 50:199–208.
8. Baird GS, Montine TJ. Multiplex immunoassay anlysis of cytokines in idiopathic inflammatory myo-pahty. Arch Pathol Lab Med. 2008; 132:232–8.
9. Bohan A, Peter JB. Polymyositis and dermatomyositis (first of two parts). N Engl J Med. 1975; 292:403–7.
10. Bohan A, Peter JB. Polymyositis and dermatomyositis (second of two parts). N Engl J Med. 1975; 292:403–7.
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