Evaluation of interleukin 13 polymorphisms in systemic sclerosis

Granel, B.; Chevillard, Christophe; Allanore, Yannick; Arnaud, Violaine; Cabantous, Stéphanie; Marquet, Sandrine; Weiller, Pierre‐Jean; Durand, J.M.; Harlé, Jean‐Robert; Grangé, C.; Francès, Y.; Berbis, P.; Gaudart, Jean; Micco, Philippe de; Kahan, André; Dessein, Alain

doi:10.1007/s00251-006-0135-0

Cited by 39 publications

(20 citation statements)

References 25 publications

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“…CD4/CD8 double-positive cells producing high levels of IL-4 were found in lesional skin of SSc patients [341]. However, no correlation with IL-4, IL-13 or their receptor gene polymorphisms was found in another study with a much larger patient cohort [342].…”

Section: Autoimmune Diseasementioning

confidence: 86%

Strategies targeting the IL-4/IL-13 axes in disease

May¹,

Fung²

2015

Cytokine

139

104

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Section: Autoimmune Diseasementioning

confidence: 86%

Strategies targeting the IL-4/IL-13 axes in disease

May¹,

Fung²

2015

Cytokine

139

104

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“…In keeping with this hypothesis, IL-13, the major fibrogenic effector at sites of Th2 responses, is elevated in the lung and circulation of patients with SSc and patients with linear scleroderma or SSc-like reactions to prosthetics (24, 57, 58). Additionally, genetic inquiries and murine modeling have provided lines of evidence that suggest that IL-13 plays a critical role in the pathogenesis of the fibrosis in SSc (59–61). We thus hypothesized that Chit1 exerts its effects by contributing to the pathogenesis of IL-13–induced fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Chitinase 1 Is a Biomarker for and Therapeutic Target in Scleroderma-Associated Interstitial Lung Disease That Augments TGF-β1 Signaling

Lee

Herzog

Ahangari

et al. 2012

The Journal of Immunology

112

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Interstitial lung disease (ILD) with pulmonary fibrosis is an important manifestation in systemic sclerosis (SSc, scleroderma) where it portends a poor prognosis. However, biomarkers that predict the development and or severity of SSc-ILD have not been validated, and the pathogenetic mechanisms that engender this pulmonary response are poorly understood. In this study, we demonstrate in two different patient cohorts that the levels of chitotriosidase (Chit1) bioactivity and protein are significantly increased in the circulation and lungs of SSc patients compared with demographically matched controls. We also demonstrate that, compared with patients without lung involvement, patients with ILD show high levels of circulating Chit1 activity that correlate with disease severity. Murine modeling shows that in comparison with wild-type mice, bleomycin-induced pulmonary fibrosis was significantly reduced in Chit1−/− mice and significantly enhanced in lungs from Chit1 overexpressing transgenic animals. In vitro studies also demonstrated that Chit1 interacts with TGF-β1 to augment fibroblast TGF-β receptors 1 and 2 expression and TGF-β–induced Smad and MAPK/ERK activation. These studies indicate that Chit1 is potential biomarker for ILD in SSc and a therapeutic target in SSc-associated lung fibrosis and demonstrate that Chit1 augments TGF-β1 effects by increasing receptor expression and canonical and noncanonical TGF-β1 signaling.

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“…One association with asthma and atopy is the IL-13 variant, Arg130Gln, that produces an IL-13 peptide that still activates the IL-13Rα1 receptor but has lower affinity for the IL-13Rα2 receptor67 giving a phenotype that would be predicted to enhance IL-13 effects 68–72. Furthermore, polymorphisms in the IL-13Rα2 gene that could affect the binding of transcription factors are significantly associated with systemic sclerosis patients69 but there are no functional data to explain any of these effects on IL-13Rα2 expression. One small study in ulcerative colitis patients failed to show disease association with the Arg130Gln IL-13 variant 72.…”

Section: Il-13 and Human Diseasementioning

confidence: 99%

Interleukin 13 and its role in gut defence and inflammation

Mannon

Reinisch

2012

Gut

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Interleukin 13 (IL-13) is a cytokine of increasing interest to gastroenterologists because of its developing role in ulcerative colitis, eosinophilic oesophagitis (EO) and fibrosis. Recent data show that IL-13 may play an important role in a novel innate immune response since it can be released by signals from an injured or inflamed epithelium, of particular relevance to the gut. Animal models of IL-13-driven inflammation (from asthma to colitis and EO) are being translated to human disease and providing insight into potential strategies for new therapies. In fact, multiple clinical trials using anti-IL-13 drugs are underway in asthma and are being extended to gastrointestinal diseases. This review presents the current knowledge on IL-13 production and function in the gut, including the cells and receptor signalling pathways involved in mediating IL-13 effects, the proposed mechanisms of IL-13 induced gut disease and the many drugs currently being tested that target IL-13 related pathways.

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Evaluation of interleukin 13 polymorphisms in systemic sclerosis

Cited by 39 publications

References 25 publications

Strategies targeting the IL-4/IL-13 axes in disease

Strategies targeting the IL-4/IL-13 axes in disease

Chitinase 1 Is a Biomarker for and Therapeutic Target in Scleroderma-Associated Interstitial Lung Disease That Augments TGF-β1 Signaling

Interleukin 13 and its role in gut defence and inflammation

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