The interferon gamma gene in celiac disease: augmented expression correlates with tissue damage but no evidence for genetic susceptibility

Wapenaar, Martin C.; Belzen, Martine J. van; Fransen, Justin H.; Sarasqueta, Aranzazu Fariña; Houwen, Roderick H. J.; Meijer, Jos W. R.; Mulder, Chris J.; Wijmenga, Cisca

doi:10.1016/j.jaut.2004.05.004

Cited by 52 publications

(37 citation statements)

References 32 publications

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“…Although GFD for one year did down regulate these markers the expression of STAT1 and IRF1 genes were still elevated in treated children with CD compared to reference children. The findings in our study are in agreement with previous reports of the increased intestinal IFN-γ and STAT1 expression in untreated CD both at RNA and protein level [7,9,[18][19][20][21][22]. Further, IRF1 which is involved in IFN-γ [23,24] and TNF mediated responses [25] via regulation of the induction of NO/iNOS in macrophages [24,26] has previously been reported to be elevated at RNA and protein level in biopsies from untreated CD children [18].…”

Section: Discussionsupporting

confidence: 92%

The effect of gluten-free diet on Th1–Th2–Th3-associated intestinal immune responses in celiac disease

Lahdenperä

Ludvigsson

Fälth‐Magnusson

et al. 2011

Scandinavian Journal of Gastroenterology

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Section: Discussionsupporting

confidence: 92%

The effect of gluten-free diet on Th1–Th2–Th3-associated intestinal immune responses in celiac disease

Lahdenperä

Ludvigsson

Fälth‐Magnusson

et al. 2011

Scandinavian Journal of Gastroenterology

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“…A correlation between the average level of IFN -γ expression and the extent of tissue restructuring in the intestinal mucosa is a fact [7]. Thus in biopsy with complete atrophy of villi (MIIIc), this expression is about 240 -fold higher than that measured in the averaged controls [7].…”

Section: B Ifn -γ In CDmentioning

confidence: 99%

Assessment of Inerferon Gamma (Ifn-Γ ) & Interleukin-10 (Il-10) in Patients Afflected with Celiac Disease

Elia¹,

Hussain²

2017

Cihan Univ.-Erbil Sci. J.

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Celiac disease (CD) is an immune mediated malabsorption syndrome that occur in genetically susceptible individuals intolerant to dietary gluten. Although considered as a primary gastrointestinal disease, CD is now known to have widespread systemic manifestation.We attempted to define the nature and role of some systemic cytokine that possibly play a role in the pathophysiology of the disease.The sera were collected from those patient suspected of having CD on clinical ground (Newly diagnosed) & then subjected to serologic tests namely anti -tissue transglutaminase IgA, IgG (tTG) & IgA, IgG -Endomysial antibody (EMA).The positive sera for anti -tTG IgA and IgA EMA autoantibody above the cutoff level were then subjected to cytokines assessment namely serum interferon gamma (IFN-γ) and interleukin-10 (IL -10) level.The participant groups comprised 50 newly diagnosed (ND) CD, 20 patients on gluten free diet (GFD) and 20 apparently healthy CD free control (These groups were subjected to the above parameters).The results of the present study among the newly diagnosed cases reveals antitTG IgA and IgA -EMA seropositivity in 15.1 % of the total 330 sera examined ;with anti-tTG IgG & IgG -EMA seronegativity (below the cut-off ) in all sera tested. The highest percent distribution of anti-tTG IgA and IgA -EMA seropositivity was at the serum concentration of 20-29 (36 % & 34 % respectively).A significant decrease (P˂ 0.01) was observed in the mean concentration of antitTG IgA and IgA-EMA between newly diagnosed CD and patients on GFD. The mean

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“…When gluten is ingested by coeliac patients, it provokes an inflammatory reaction in the small intestine that leads to crypt hyperplasia and villous atrophy. 1 Although the exact nature of this immune response remains unknown, there is much evidence to suggest that gluten promotes a Th1 immune response mostly mediated by high levels of interferon-gamma (IFN-g) 2 and ab CD4 þ T cells that recognize gluten peptides through HLA-DQ2/DQ8 molecules. 3 This observation is further supported by genetic data showing a primary association between the genes encoding the HLA-DQ2/DQ8 molecules on chromosome 6 and all the CD populations tested to date.…”

Section: Introductionmentioning

confidence: 99%

“…8 -10 One interesting activator of the JAK-STAT pathway in CD might be IFN-g, which is also highly expressed in the intestine of coeliac individuals. 2 The exact role of IFN-g in the pathogenesis of CD has not been elucidated, but it might contribute to the maintenance of the chronic inflammatory response through the JAK-STAT pathway by regulating the expression and the activation of STAT1.…”

Section: Introductionmentioning

confidence: 99%

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The downstream modulator of interferon-γ, STAT1 is not genetically associated to the Dutch coeliac disease population

et al. 2006

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Coeliac disease (CD) is a complex genetic disorder. Its etiology is owing to multiple genes and environmental factors, such as gluten. The first event in the pathogenesis of CD after the ingestion of gluten is the activation of a Th1 immune response that leads to villous atrophy. Although this immune response seems crucial to the disease's development, only the HLA-DQ2/DQ8 genes have been identified as causative immune genes related to CD. Recently, the activation of the transcription factor STAT1 and changes in its expression levels have confirmed the participation of the Janus kinase-signal transducer and activator of transcription pathway in CD. Furthermore, as the STAT-1 gene is a positional candidate located in the CELIAC3 locus on chromosome 2, we speculate that alterations in this gene could be primarily responsible for the aberrant immune response that characterizes CD. Based on this functional and genetic evidence, we investigated the primary contribution of STAT-1 to CD. We performed a comprehensive genetic association study using five tag SNPs fully covering the STAT-1 gene in a Dutch cohort of 355 independent CD cases and 360 healthy controls. Neither the alleles, nor the genotypes in the case -control genetic association studies, nor the haplotype analysis showed any association to the STAT-1 gene in the Dutch CD population. Our results do not point to a primary involvement of the STAT-1 gene in the Dutch CD population.

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The interferon gamma gene in celiac disease: augmented expression correlates with tissue damage but no evidence for genetic susceptibility

Cited by 52 publications

References 32 publications

The effect of gluten-free diet on Th1–Th2–Th3-associated intestinal immune responses in celiac disease

The effect of gluten-free diet on Th1–Th2–Th3-associated intestinal immune responses in celiac disease

Assessment of Inerferon Gamma (Ifn-Γ ) & Interleukin-10 (Il-10) in Patients Afflected with Celiac Disease

The downstream modulator of interferon-γ, STAT1 is not genetically associated to the Dutch coeliac disease population

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