Advanced search
1 file | 791.62 KB Add to list

Scanning for therapeutic targets within the cytokine network of idiopathic inflammatory myopathies

Author
Organization
Abstract
The idiopathic inflammatory myopathies (IIM) constitute a heterogeneous group of chronic disorders that include dermatomyositis (DM), polymyositis (PM), sporadic inclusion body myositis (IBM) and necrotizing autoimmune myopathy (NAM). They represent distinct pathological entities that, most often, share predominant inflammation in muscle tissue. Many of the immunopathogenic processes behind the IIM remain poorly understood, but the crucial role of cytokines as essential regulators of the intramuscular build-up of inflammation is undisputed. This review describes the extensive cytokine network within IIM muscle, characterized by strong expression of Tumor Necrosis Factors (TNF, LT, BAFF), Interferons (IFN//), Interleukins (IL-1/6/12/15/18/23) and Chemokines (CXCL9/10/11/13, CCL2/3/4/8/19/21). Current therapeutic strategies and the exploration of potential disease modifying agents based on manipulation of the cytokine network are provided. Reported responses to anti-TNF treatment in IIM are conflicting and new onset DM/PM has been described after administration of anti-TNF agents to treat other diseases, pointing to the complex effects of TNF neutralization. Treatment with anti-IFN has been shown to suppress the IFN type 1 gene signature in DM/PM patients and improve muscle strength. Beneficial effects of anti-IL-1 and anti-IL-6 therapy have also been reported. Cytokine profiling in IIM aids the development of therapeutic strategies and provides approaches to subtype patients for treatment outcome prediction.
Keywords
TERM-FOLLOW-UP, SEVERE CROHNS-DISEASE, CHRONIC PLAQUE PSORIASIS, IL-1 RECEPTOR ANTAGONIST, INTERSTITIAL LUNG-DISEASE, CYTOSOLIC 5'-NUCLEOTIDASE 1A, INTERLEUKIN-12/23 MONOCLONAL-ANTIBODY, MEDIATED NECROTIZING MYOPATHY, NECROSIS-FACTOR-ALPHA, INCLUSION-BODY MYOSITIS, tumor necrosis factor, tocilizumab, sifalimumab, infliximab, dermatomyositis, etanercept, inflammatory myopathy, anakinra, avonex, cytokine

Downloads

  • 2015IJMS.pdf
    • full text
    • |
    • open access
    • |
    • PDF
    • |
    • 791.62 KB

Citation

Please use this url to cite or link to this publication:

MLA
De Paepe, Boel, and Jana Zschüntzsch. “Scanning for Therapeutic Targets within the Cytokine Network of Idiopathic Inflammatory Myopathies.” INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, vol. 16, no. 8, 2015, pp. 18683–713, doi:10.3390/ijms160818683.
APA
De Paepe, B., & Zschüntzsch, J. (2015). Scanning for therapeutic targets within the cytokine network of idiopathic inflammatory myopathies. INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 16(8), 18683–18713. https://doi.org/10.3390/ijms160818683
Chicago author-date
De Paepe, Boel, and Jana Zschüntzsch. 2015. “Scanning for Therapeutic Targets within the Cytokine Network of Idiopathic Inflammatory Myopathies.” INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES 16 (8): 18683–713. https://doi.org/10.3390/ijms160818683.
Chicago author-date (all authors)
De Paepe, Boel, and Jana Zschüntzsch. 2015. “Scanning for Therapeutic Targets within the Cytokine Network of Idiopathic Inflammatory Myopathies.” INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES 16 (8): 18683–18713. doi:10.3390/ijms160818683.
Vancouver
1.
De Paepe B, Zschüntzsch J. Scanning for therapeutic targets within the cytokine network of idiopathic inflammatory myopathies. INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES. 2015;16(8):18683–713.
IEEE
[1]
B. De Paepe and J. Zschüntzsch, “Scanning for therapeutic targets within the cytokine network of idiopathic inflammatory myopathies,” INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, vol. 16, no. 8, pp. 18683–18713, 2015.
@article{7038312,
  abstract     = {{The idiopathic inflammatory myopathies (IIM) constitute a heterogeneous group of chronic disorders that include dermatomyositis (DM), polymyositis (PM), sporadic inclusion body myositis (IBM) and necrotizing autoimmune myopathy (NAM). They represent distinct pathological entities that, most often, share predominant inflammation in muscle tissue. Many of the immunopathogenic processes behind the IIM remain poorly understood, but the crucial role of cytokines as essential regulators of the intramuscular build-up of inflammation is undisputed. This review describes the extensive cytokine network within IIM muscle, characterized by strong expression of Tumor Necrosis Factors (TNF, LT, BAFF), Interferons (IFN//), Interleukins (IL-1/6/12/15/18/23) and Chemokines (CXCL9/10/11/13, CCL2/3/4/8/19/21). Current therapeutic strategies and the exploration of potential disease modifying agents based on manipulation of the cytokine network are provided. Reported responses to anti-TNF treatment in IIM are conflicting and new onset DM/PM has been described after administration of anti-TNF agents to treat other diseases, pointing to the complex effects of TNF neutralization. Treatment with anti-IFN has been shown to suppress the IFN type 1 gene signature in DM/PM patients and improve muscle strength. Beneficial effects of anti-IL-1 and anti-IL-6 therapy have also been reported. Cytokine profiling in IIM aids the development of therapeutic strategies and provides approaches to subtype patients for treatment outcome prediction.}},
  author       = {{De Paepe, Boel and Zschüntzsch, Jana}},
  issn         = {{1422-0067}},
  journal      = {{INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES}},
  keywords     = {{TERM-FOLLOW-UP,SEVERE CROHNS-DISEASE,CHRONIC PLAQUE PSORIASIS,IL-1 RECEPTOR ANTAGONIST,INTERSTITIAL LUNG-DISEASE,CYTOSOLIC 5'-NUCLEOTIDASE 1A,INTERLEUKIN-12/23 MONOCLONAL-ANTIBODY,MEDIATED NECROTIZING MYOPATHY,NECROSIS-FACTOR-ALPHA,INCLUSION-BODY MYOSITIS,tumor necrosis factor,tocilizumab,sifalimumab,infliximab,dermatomyositis,etanercept,inflammatory myopathy,anakinra,avonex,cytokine}},
  language     = {{eng}},
  number       = {{8}},
  pages        = {{18683--18713}},
  title        = {{Scanning for therapeutic targets within the cytokine network of idiopathic inflammatory myopathies}},
  url          = {{http://doi.org/10.3390/ijms160818683}},
  volume       = {{16}},
  year         = {{2015}},
}

Altmetric
View in Altmetric
Web of Science
Times cited: