Given the known involvement of IL-36 in psoriasis it might be surprising that the latest mouse models show that inhibiting IL-36 signalling does not alter the course of inflammatory arthritis. Can we now add IL-36 to the list of inflammatory mediators that are not viable DMARD targets?
This is a preview of subscription content, access via your institution
Relevant articles
Open Access articles citing this article.
-
The relationship of indoxyl sulfate and p-cresyl sulfate with target cardiovascular proteins in hemodialysis patients
Scientific Reports Open Access 15 February 2021
-
Mutations in IL36RN are associated with geographic tongue
Human Genetics Open Access 29 November 2016
-
Ambient particulate matter and microRNAs in extracellular vesicles: a pilot study of older individuals
Particle and Fibre Toxicology Open Access 08 March 2016
Access options
Subscribe to this journal
Receive 12 print issues and online access
$209.00 per year
only $17.42 per issue
Buy this article
- Purchase on Springer Link
- Instant access to full article PDF
Prices may be subject to local taxes which are calculated during checkout
References
Derer, A. et al. Blockade of IL-36 receptor signaling does not prevent from TNF-induced arthritis. PLoS ONE 9, e101954 (2014).
Sims J. E., Vigne S., Gabay C. & Towne J. in Cytokine Frontiers: Regulation of Immune Response in Health and Disease. (eds Yoshimoto, T. & Yoshimoto, T.) 199–214 (Springer, 2014).
Vigne, S. et al. IL-36R ligands are potent regulators of dendritic and T cells. Blood 118, 5813–5823 (2011).
Foster, A. M. et al. IL-36 promotes myeloid cell infiltration, activation, and inflammatory activity in skin. J. Immunol. 192, 6053–6061 (2014).
Vigne, S. et al. IL-36 signaling amplifies TH1 responses by enhancing proliferation and TH1 polarization of naive CD4+ T cells. Blood 120, 3478–3487 (2012).
Frey, S. et al. The novel cytokine interleukin-36α is expressed in psoriatic and rheumatoid arthritis synovium. Ann. Rheum. Dis. 72, 1569–1574 (2013).
Magne, D. et al. The new IL-1 family member IL-1F8 stimulates production of inflammatory mediators by synovial fibroblasts and articular chondrocytes. Arthritis Res. Ther. 8, R80 (2006).
Lamacchia, C. et al. The severity of experimental arthritis is independent of IL-36 receptor signaling. Arthritis Res. Ther. 15, R38 (2013).
Tortola, L. et al. Psoriasiform dermatitis is driven by IL-36-mediated DC-keratinocyte crosstalk. J. Clin. Invest. 122, 3965–3976 (2012).
Marrakchi, S. et al. Interleukin-36-receptor antagonist deficiency and generalized pustular psoriasis. N. Engl. J. Med. 365, 620–628 (2011).
Acknowledgements
The authors acknowledge that they are supported by a grant from the Swiss National Science Foundation (No. 310030_152638), the Rheumasearch Foundation and the Institute of Arthritis Research.
Author information
Authors and Affiliations
Corresponding author
Ethics declarations
Competing interests
The authors declare no competing financial interests.
PowerPoint slides
Rights and permissions
About this article
Cite this article
Dietrich, D., Gabay, C. IL-36 has proinflammatory effects in skin but not in joints. Nat Rev Rheumatol 10, 639–640 (2014). https://doi.org/10.1038/nrrheum.2014.156
Published:
Issue Date:
DOI: https://doi.org/10.1038/nrrheum.2014.156
This article is cited by
-
The relationship of indoxyl sulfate and p-cresyl sulfate with target cardiovascular proteins in hemodialysis patients
Scientific Reports (2021)
-
Mutations in IL36RN are associated with geographic tongue
Human Genetics (2017)
-
Ambient particulate matter and microRNAs in extracellular vesicles: a pilot study of older individuals
Particle and Fibre Toxicology (2015)