Infiltration of forkhead box P3-expressing cells in small intestinal mucosa in coeliac disease but not in type 1 diabetes

Tiittanen, Minna; Westerholm-Ormio, Mia; Verkasalo, M; Savilahti, Erkki; Vaarala, Outi

doi:10.1111/j.1365-2249.2008.03662.x

Cited by 82 publications

(84 citation statements)

References 41 publications

(52 reference statements)

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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: 83%

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: 83%

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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“…Studies have demonstrated that the number of CD4 1 CD25 1 FoxP3 1 regulatory T cells is increased in the small-bowel mucosa of CD patients; this increase might represent a compensatory mechanism to downregulate the elevated immune response to foreign and self-antigens. [13][14][15] Immune responses to the self-antigen tTG may be caused by the increased expression of tTG in the intestinal mucosa, 16 a conformational change in enzyme structure 17 or the release of intracellular tTG that, when picked up by dendritic cells, subsequently leads to the activation of adaptive immune responses. Antibodies against tTG may influence either the deamidating or the transamidating activity of the enzyme, which may lead to significant biological effects in intestine.…”

Section: Introductionmentioning

confidence: 99%

Celiac disease in patients with type 1 diabetes: a condition with distinct changes in intestinal immunity?

et al. 2011

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Two common chronic childhood diseases-celiac disease (CD) and type 1 diabetes (T1D)-result from complex pathological mechanisms where genetic susceptibility, environmental exposure, alterations in intestinal permeability and immune responses play central roles. In this study, we investigated whether these characteristics were universal for CD independently of T1D association. For this purpose, we studied 36 children with normal small-bowel mucosa and 26 children with active CD, including 12 patients with T1D. In samples from the small-bowel mucosa, we detected the lowest expression of tight junction protein 1 (TJP1) mRNA in CD patients with T1D, indicating an increase in intestinal permeability. Furthermore, these samples displayed the highest expression of forkhead box P3 (FoxP3) mRNA, a marker for regulatory T cells, as compared with other patient groups. At the same time, serum levels of IgA antibodies specific for the CD-related antigens deamidated gliadin and tissue transglutaminase (tTG) were the highest in CD patients with T1D. In contrast, no significant differences were found in IgA or IgG antibodies specific for bovine beta-lactoglobulin or Bifidobacterium adolescentis DSM 20083-derived proteins. There were also no differences in the transamidating activity of serum autoantibodies between patients and control individuals. Our results show that patients with T1D and newly detected CD exhibit severely altered intestinal permeability, strong local immune activation and increased immunoregulatory mechanisms in the small bowel. Further study is required to determine whether these extreme changes in this CD subgroup are due to some specific environmental factors (virus infections), unknown genetic effects or autoimmune reactions to antigenic targets in intracellular tight junctions. INTRODUCTIONWith an approximate prevalence of 1.0% in Western countries, celiac disease (CD) is one of the most common lifelong chronic disorders. 1 CD and type 1 diabetes (T1D) form a significant sector of childhood diseases with high rate of co-occurrence. 2 Both diseases are autoimmune in origin and develop as a result of complex pathological mechanisms, involving several common genetic, environmental and immunological factors. Among these, the common susceptibility loci of HLA and other immune system-related genes, 3 permeability changes in the small-bowel mucosa, 4 and association with wheat consumption 4,5 are prominent. Both diseases are increasing in most regions of the world, 6,7 as are several other autoimmune diseases, but the actual cause of the disease remains unknown. However, several recent studies have highlighted the role of environmental and social changes that have taken place over the last several decades. 8,9 The central event in the pathogenesis of CD is damage to the small intestinal mucosa that occurs after ingestion of gluten or related prolamins in genetically susceptible individuals. During this process, several morphological and immunological alterations have been demonstrated in the small-bowel mucos...

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“…In both CD and T1D intestinal inflammation has been observed as altered mucosal cytokine expression and increased activation of intestinal T lymphocytes [1][2][3]. Intestinal inflammation in CD is characterized by villous atrophy and crypt hyperplasia, which is not seen in T1D.…”

Section: Introductionmentioning

confidence: 99%

“…Previously increased small intestinal immune activation seen as increased numbers of HLA class II-, CD25-, MadCAM-1-, IL-1a-and IL-4-positive cells has been reported in T1D [1][2][3]. Accumulating evidence suggests intestinal inflammation as part of the disease pathogenesis [17,18].…”

Section: Introductionmentioning

confidence: 99%

Up-regulation of small intestinal interleukin-17 immunity in untreated coeliac disease but not in potential coeliac disease or in type 1 diabetes

Lahdenperä

Hölttä

Ruohtula

et al. 2012

Clinical and Experimental Immunology

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Infiltration of forkhead box P3-expressing cells in small intestinal mucosa in coeliac disease but not in type 1 diabetes

Cited by 82 publications

References 41 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

Celiac disease in patients with type 1 diabetes: a condition with distinct changes in intestinal immunity?

Up-regulation of small intestinal interleukin-17 immunity in untreated coeliac disease but not in potential coeliac disease or in type 1 diabetes

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