Serum IL-17, BMP-7, and bone turnover markers in patients with ankylosing spondylitis

Wendling, Daniel; Cedoz, Jean-Pierre; Racadot, E; Dumoulin, Gilles

doi:10.1016/j.jbspin.2006.11.005

Cited by 160 publications

(116 citation statements)

References 7 publications

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“…This study confirms previous observations of an elevated Th17 axis in AS patients (7,23). We have now provided additional insights by demonstrating that the increased frequency of IL-17A and Th17 cells is a malerelated immune event.…”

Section: Discussionsupporting

confidence: 90%

Sexual Dimorphism in the Th17 Signature of Ankylosing Spondylitis

Gracey

Yao

Green

et al. 2016

Arthritis & Rheumatology

144

101

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ObjectiveTo identify an immunologic basis for the male sex bias in ankylosing spondylitis (AS).MethodsCohorts of male and female patients with AS and age‐ and sex‐matched healthy control subjects were selected, and the levels of serum cytokines (interferon‐γ [IFNγ], tumor necrosis factor α, interleukin‐17A [IL‐17A], and IL‐6) were examined by enzyme‐linked immunosorbent assay, the frequencies of Th1 and Th17 cells were assessed by flow cytometry, and whole blood gene expression was analyzed using both microarray and NanoString approaches.ResultsThe frequency of IL‐17A and Th17 cells, both of which are key factors in the inflammatory Th17 axis, was elevated in male patients with AS but not in female patients with AS. In contrast, AS‐associated alterations in the Th1 axis, such as the frequency of IFNγ and Th1 cells in serum, were independent of a patient's sex. Results of microarray analysis supported an altered Th17 axis in male patients, with a specific increase in IL17RA. In addition, male and female patients with AS displayed shared gene expression patterns, while male patients with AS had additional alterations in gene expression that were not seen in female patients with AS. The differential sex‐related immune profiles were independent of HLA–B27 status, clinical disease activity (as measured by the Bath Ankylosing Spondylitis Disease Activity Index), or treatment (with nonsteroidal antiinflammatory drugs or biologic agents), implicating intrinsic sexual dimorphism in AS.ConclusionThe results of this study demonstrate distinct sexual dimorphism in the activation status of the immune system in patients with AS, particularly in the Th17 axis. This dimorphism could underlie sex‐related differences in the clinical features of AS and could provide a rationale for sex‐specific treatment of AS.

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Section: Discussionsupporting

confidence: 90%

Sexual Dimorphism in the Th17 Signature of Ankylosing Spondylitis

Gracey

Yao

Green

et al. 2016

Arthritis & Rheumatology

144

101

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“…These cells exhibit a highly differentiated and polyfunctional phenotype in SpA, suggesting a specific role of Th17 cells in these diseases. Consistent with these results, increased levels of IL-17 in the sera of AS patients have been previously identified in studies using Quantikine ELISA (27). Unexpectedly, Th17 cell frequencies were comparable in RA patients and healthy donors, suggesting that Th17 cells may not be as central to the pathogenesis of RA as concluded from animal models (18).…”

Section: Discussionsupporting

confidence: 83%

Increased numbers of circulating polyfunctional Th17 memory cells in patients with seronegative spondylarthritides

Jandus¹,

Bioley²,

Rivals³

et al. 2008

Arthritis & Rheumatism

350

229

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Objective. A distinct subset of proinflammatory CD4؉ T cells that produce interleukin-17 was recently identified. These cells are implicated in different autoimmune disease models, such as experimental autoimmune encephalomyelitis and collagen-induced arthritis, but their involvement in human autoimmune disease has not yet been clearly established. The purpose of this study was to assess the frequency and functional properties of Th17 cells in healthy donors and in patients with different autoimmune diseases.Methods. Peripheral blood was obtained from 10 psoriatic arthritis (PsA), 10 ankylosing spondylitis (AS), 10 rheumatoid arthritis (RA), and 5 vitiligo patients, as well as from 25 healthy donors. Synovial tissue samples from a separate group of patients were also evaluated (obtained as paraffin-embedded sections). Peripheral blood cells were analyzed by multiparameter flow cytometry and immunohistochemistry. Cytokine production was examined by enzyme-linked immunosorbent assay and intracellular cytokine staining using specific monoclonal antibodies. Synovial tissue was examined for infiltrating T cells by immunohistochemical analysis.Results. We found increased numbers of circulating Th17 cells in the peripheral blood of patients with seronegative spondylarthritides (PsA and AS), but not in patients with RA or vitiligo. In addition, Th17 cells from the spondylarthritis patients showed advanced differentiation and were polyfunctional in terms of T cell receptor-driven cytokine production.Conclusion. These observations suggest a role of Th17 cells in the pathogenesis of certain human autoimmune disorders, in particular the seronegative spondylarthritides.

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“…IL-17A is an effector cytokine requiring IL-23 signaling, which has been implicated in the pathogenesis of SpA and Crohn's disease (8)(9)(10)28,29). To determine the role of IL-17A in the development of SpA and ileitis in SKG mice, we generated IL-17A Ϫ/Ϫ SKG mice and injected them IP with curdlan.…”

Section: Methodsmentioning

confidence: 99%

Interleukin‐23 Mediates the Intestinal Response to Microbial β‐1,3‐Glucan and the Development of Spondyloarthritis Pathology in SKG Mice

Benham

Rehaume

Hasnain

et al. 2014

Arthritis & Rheumatology

187

125

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Results. In curdlan-treated SKG mice, arthritis, enthesitis, and ileitis were IL-23 dependent. Enthesitis was specifically dependent on IL-17A and IL-22. IL-23 was induced in the ileum, where it amplified ER stress, goblet cell dysfunction, and proinflammatory cytokine production. IL-17A was pathogenic, while IL-22 was protective against ileitis. IL-22؉CD3؊ innate-like cells were increased in lamina propria mononuclear cells of ileitis-resistant BALB/c mice, which developed ileitis after curdlan injection and anti-IL-22.Conclusion. In response to systemic ␤-1,3-glucan, intestinal IL-23 provokes local mucosal dysregulation and cytokines driving the SpA syndrome, including IL-17/IL-22-dependent enthesitis. Innate IL-22 production promotes ileal tolerance.

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Serum IL-17, BMP-7, and bone turnover markers in patients with ankylosing spondylitis

Cited by 160 publications

References 7 publications

Sexual Dimorphism in the Th17 Signature of Ankylosing Spondylitis

Sexual Dimorphism in the Th17 Signature of Ankylosing Spondylitis

Increased numbers of circulating polyfunctional Th17 memory cells in patients with seronegative spondylarthritides

Interleukin‐23 Mediates the Intestinal Response to Microbial β‐1,3‐Glucan and the Development of Spondyloarthritis Pathology in SKG Mice

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