Overexpression of interleukin‐23, but not interleukin‐17, as an immunologic signature of subclinical intestinal inflammation in ankylosing spondylitis

Ciccia, Francesco; Bombardieri, Michèle; Principato, Alfonso; Giardina, A; Tripodo, Claudio; Porcasi, Rossana; Peralta, Sergio; Franco, Vito; Giardina, E; Craxı̀, Antonio; Pitzalis, Costantino; Triolo, G

doi:10.1002/art.24389

Cited by 209 publications

(160 citation statements)

References 40 publications

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“…These cells are present with a specific tissue distribution and could play a vital function in the development or progression of SpA-related pathology [33]. Moreover, there is evidence for increased IL-23 expression in inflamed tissues including the gut of SpA patients without an overt IBD [34]. Interestingly, IL-17 was not significantly upregulated in AS, nor were IL-6 and IL-1β, whereas these cytokines were overexpressed in subjects with CD.…”

Section: Enteropathic Spa: Insights On the Pathogenesismentioning

confidence: 99%

Impact of a multidisciplinary approach in enteropathic spondyloarthritis patients

Conigliaro

Chimenti

Ascolani

et al. 2016

Autoimmunity Reviews

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Spondyloarthritis (SpA) and inflammatory bowel disease (IBD) are chronic autoinflammatory diseases that partially share the genetic predisposition and the unchecked inflammatory response linking the gut to the joints. The coexistence of both conditions in patients and the increased cross-risk ratios between SpA and IBD strongly suggest a shared pathophysiology. The prevalence of Enteropathic-related Spondyloarthritis (ESpA) in IBD patients shows a wide variation and may be underestimated. It is well accepted that the management of joint pain requires rheumatological expertise in conjunction with gastroenterologist assessment. In this view, we aimed at assessing, in a prospective study performed in a combined Gastro-Intestinal and Rheumatologic "GI-Rhe" clinic: (1) the prevalence of ESpA and other rheumatologic diseases in IBD patients with joint pain; (2) the features of the ESpA population; and (3) the diagnostic delay and the potential impact of the combined assessment. From November 2012 to December 2014, IBD patients with joint pain referring to a dedicated rheumatologist by the IBD-dedicated gastroenterologist were enrolled. Clinical and biochemical evaluations, joint involvement and disease activity assessment, diagnostic delay, and treatment were recorded. IBD patients (n = 269) with joint pain were jointly assessed in the "GI-Rhe" Unit. A diagnosis of ESpA was made in 50.5% of IBD patients with joint pain. ESpA patients showed a peripheral involvement in 53% of cases, axial in 20.6% and peripheral and axial in 26.4% of cases. ESpA patients had a higher prevalence of other autoimmune extra-intestinal manifestations and received more anti-TNF treatment compared with IBD patients. A mean diagnostic delay of 5.2 years was revealed in ESpA patients. Patients with joint disease onset in the 2002-2012 decade had reduced diagnostic delay compared with those with onset in the 1980-1990 and 1991-2001 decades. Diagnostic delay was further reduced for patients with joint onset in the last two years in conjunction with the establishment of the GI-Rhe clinic. Multidisciplinary approach improved management of rheumatic disorders in IBD patients allowing a more comprehensive care.

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Section: Enteropathic Spa: Insights On the Pathogenesismentioning

confidence: 99%

Impact of a multidisciplinary approach in enteropathic spondyloarthritis patients

Conigliaro

Chimenti

Ascolani

et al. 2016

Autoimmunity Reviews

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“…APCs such as macrophages and dendritic cells, appear to be the main cellular sources of IL-23 although other studies have shown the expression of this cytokine in a variety of cell types such as microglia [91] and Paneth cells [92]. Initial studies on the biological functions of this cytokine proposed an overlapping action with IL-12 as inducer of IFNproducing Th1 cells.…”

Section: Il-23 Binds a Receptor Composed Of Il-12rβ1 And A Second Submentioning

confidence: 99%

From IL-15 to IL-33: the never-ending list of new players in inflammation. Is it time to forget the humble aspirin and move ahead?

D’Acquisto

Μaione

Pederzoli-Ribeil

2010

Biochemical Pharmacology

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“…XBP1 mRNA is translated into a functional protein after activation of the ribonuclease domain of inositol-requiring enzyme 1␣ (IRE1␣) and excision of a 26-nucleotide unconventional intron from XBP1 mRNA that causes a frameshift in the XBP1 coding sequence resulting in the translation of the functional transcription factor. The UPR has been associated with the enhanced production of IL-23 in the pathogenesis of ankylosing spondylitis due to the accumulation of misfolded HLA-B27 heavy-chain homodimers in monocytes and lymphocytes (11,12). In this study, we have carried out a comprehensive analysis of the mechanisms involved in the transcriptional regulation of il23a in human monocyte-derived dendritic cells (DC).…”

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confidence: 99%

The Unfolded Protein Response and the Phosphorylations of Activating Transcription Factor 2 in the trans-Activation of il23a Promoter Produced by β-Glucans

Rodríguez

Domingo

Alonso

et al. 2014

Journal of Biological Chemistry

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Background: Phagocytosis and Th17 immune response control fungal invasion. Results: ␤-Glucans mobilize nuclear C/EBP homologous protein (CHOP) and increase activating transcription factor 2 (ATF2) binding to the il23a promoter. Conclusion: ␤-Glucans direct proapoptotic CHOP to phagosomal vesicles and induce ATF2-dependent il23a transcription. Significance: The mechanisms underlying the unfolded protein response and the trans-activation of il23a elicited by ␤-glucans are ascertained.

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Overexpression of interleukin‐23, but not interleukin‐17, as an immunologic signature of subclinical intestinal inflammation in ankylosing spondylitis

Cited by 209 publications

References 40 publications

Impact of a multidisciplinary approach in enteropathic spondyloarthritis patients

Impact of a multidisciplinary approach in enteropathic spondyloarthritis patients

From IL-15 to IL-33: the never-ending list of new players in inflammation. Is it time to forget the humble aspirin and move ahead?

The Unfolded Protein Response and the Phosphorylations of Activating Transcription Factor 2 in the trans-Activation of il23a Promoter Produced by β-Glucans

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