Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Editorial
. 2011 Jun 24;13(3):115.
doi: 10.1186/ar3351.

IL-17 in spondyloarthritis: is the T-party over?

Nataliya Yeremenko, Dominique Baeten
Editorial

IL-17 in spondyloarthritis: is the T-party over?

Nataliya Yeremenko et al. Arthritis Res Ther. .

Abstract

The past decade has witnessed significant progress in revealing an important role for IL-17 in the pathogenesis of several immune-mediated inflammatory diseases. Recent studies have provided new insights into the cellular source of IL-17, originally identified as the signature cytokine of a distinct CD4(+) T-cell subset known as Th17. Accumulating evidence suggests that the majority of the IL-17 released in inflammatory arthritis is produced by innate immune cells rather than T cells. Understanding molecular mechanisms behind these early innate immune responses will be the key to designing rational therapies targeting these important inflammatory pathways.

PubMed Disclaimer

Comment on

References

    1. Appel H, Maier R, Wu P, Scheer R, Hempfing A, Kayser R, Thiel A, Radbruch A, Loddenkemper C, Sieper J. Analysis of interleukin-17+ cells in facet joints of patients with spondyloarthritis suggests that the innate immune pathway might be of greater relevance than the Th17 mediated adaptive immune response. Arthritis Res Ther. 2011;13:R95. doi: 10.1186/ar3370. - DOI - PMC - PubMed
    1. Di Meglio P, Di Cesare A, Laggner U, Chu CC, Napolitano L, Villanova F, Tosi I, Capon F, Trembath RC, Peris K, Nestle FO. The IL-23R R381Q gene variant protects against immune-mediated diseases by impairing IL-23-induced Th17 effector response in humans. PLoS One. 2011;6:e17160. doi: 10.1371/journal.pone.0017160. - DOI - PMC - PubMed
    1. Sarin R, Wu X, Abraham C. Inflammatory disease protective R381Q IL23 receptor polymorphism results in decreased primary CD4+ and CD8+ human T-cell functional responses. Proc Natl Acad Sci USA. 2011;108:9560–9565. doi: 10.1073/pnas.1017854108. - DOI - PMC - PubMed
    1. DeLay ML, Turner MJ, Klenk EI, Smith JA, Sowders DP, Colbert RA. HLA-B27 misfolding and the unfolded protein response augment interleukin-23 production and are associated with Th17 activation in transgenic rats. Arthritis Rheum. 2009;60:2633–2643. doi: 10.1002/art.24763. - DOI - PMC - PubMed
    1. Baeten D, Sieper J, Emery P, Braun J, van der Heijde D, McInnes I, van Laar J, Landewe R, Wordsworth P, Wollenhaupt J, Kellner H, Paramarta J, Bertolino A, Wright A, Hueber W. The anti-IL17A monoclonal antibody secukinumab (AIN457) showed good safety and efficacy in the treatment of active ankylosing spondylitis. Arthritis Rheum. 2010;62:2840–2841.

MeSH terms