Enrichment of circulating interleukin-17-secreting interleukin-23 receptor-positive γ/δ T cells in patients with active ankylosing spondylitis

Kenna, Tony J., Davidson, Stuart I., Duan, Ran, Bradbury, Linda A., McFarlane, Janelle, Smith, Malcom, Weedon, Helen, Street, Shayna, Thomas, Ranjeny, Thomas, Gethin P., & Brown, Matthew A. (2012) Enrichment of circulating interleukin-17-secreting interleukin-23 receptor-positive γ/δ T cells in patients with active ankylosing spondylitis. Arthritis and Rheumatism, 64(5), pp. 1420-1429.

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Ankylosing spondylitis (AS) is a common inflammatory arthritis affecting primarily the axial skeleton. IL23R is genetically associated with AS. This study was undertaken to investigate and characterize the role of interleukin-23 (IL-23) signaling in AS pathogenesis.


The study population consisted of patients with active AS (n = 17), patients with psoriatic arthritis (n = 8), patients with rheumatoid arthritis, (n = 9), and healthy subjects (n = 20). IL-23 receptor (IL-23R) expression in T cells was determined in each subject group, and expression levels were compared.


The proportion of IL-23R-expressing T cells in the periphery was 2-fold higher in AS patients than in healthy controls, specifically driven by a 3-fold increase in IL-23R-positive γ/δ T cells in AS patients. The proportions of CD4+ and CD8+ cells that were positive for IL-17 were unchanged. This increased IL-23R expression on γ/δ T cells was also associated with enhanced IL-17 secretion, with no observable IL-17 production from IL-23R-negative γ/δ T cells in AS patients. Furthermore, γ/δ T cells from AS patients were heavily skewed toward IL-17 production in response to stimulation with IL-23 and/or anti-CD3/CD28.


Recently, mouse models have shown IL-17-secreting γ/δ T cells to be pathogenic in infection and autoimmunity. Our data provide the first description of a potentially pathogenic role of these cells in a human autoimmune disease. Since IL-23 is a maturation and growth factor for IL-17-producing cells, increased IL-23R expression may regulate the function of this putative pathogenic γ/δ T cell population.

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ID Code: 87778
Item Type: Journal Article
Refereed: Yes
Keywords: CD161 antigen, CD28 antigen, CD3 antigen, chemokine receptor CCR6, gamma interferon, interleukin 17, interleukin 23, interleukin 23 receptor, adult, aged, ankylosing spondylitis, antigen expression, article, autoimmunity, CD4+ T lymphocyte, CD8+ T lymphocyte, cell function, cell maturation, clinical article, controlled study, cytokine production, cytokine release, female, gamma delta T lymphocyte, human, human cell, male, pathogenesis, peripheral blood mononuclear cell, priority journal, protein expression, psoriatic arthritis, rheumatoid arthritis, signal transduction, Th17 cell, Arthritis, Psoriatic, Arthritis, Rheumatoid, CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Cells, Cultured, Cytokines, Humans, Interleukin-17, Leukocytes, Mononuclear, Middle Aged, Receptors, Antigen, T-Cell, gamma-delta, Receptors, Interleukin, Spondylitis, Ankylosing, Young Adult
DOI: 10.1002/art.33507
ISSN: 0004-3591
Divisions: Current > Schools > School of Biomedical Sciences
Current > QUT Faculties and Divisions > Faculty of Health
Current > Institutes > Institute of Health and Biomedical Innovation
Deposited On: 28 Sep 2015 05:16
Last Modified: 24 Mar 2016 03:52

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