Intraepithelial Lymphocytes in Celiac Disease

Järvinen, Teea T; Kaukinen, Katri; Laurila, Kaija; Kyrönpalo, Sinikka; Rasmussen, Martin; Mäki, Markku; Korhonen, Heikki; Reunala, Timo; Collin, Pekka

doi:10.1111/j.1572-0241.2003.07456.x

Cited by 129 publications

(91 citation statements)

References 25 publications

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“…We chose to investigate the possible role of CXCR3 as a receptor for gliadin because of its function in recruiting γ/δ lymphocytes, a marker of early stage in CD pathogenesis. 26 In contrast, the glutamate receptor is an intrinsic transmembrane ion channel that is opened in response to binding of a chemical messenger but has not been described to be involved in cell activation and rearrangement of the cytoskeleton. 21 Heat shock proteins are cytoplasmic proteins involved in intracellular processes including protein folding and protein conformation and are found extracellularly only as shed contents from necrotic cells providing a strong danger signal to the immune system.…”

Section: Discussionmentioning

confidence: 99%

Gliadin Induces an Increase in Intestinal Permeability and Zonulin Release by Binding to the Chemokine Receptor CXCR3

et al. 2008

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Background & Aims-Celiac disease is an immune-mediated enteropathy triggered by gliadin, a component of the grain protein gluten. Gliadin induces an MyD88-dependent zonulin release that leads to increased intestinal permeability, a postulated early element in the pathogenesis of celiac disease. We aimed to establish the molecular basis of gliadin interaction with intestinal mucosa leading to intestinal barrier impairment.

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Section: Discussionmentioning

confidence: 99%

Gliadin Induces an Increase in Intestinal Permeability and Zonulin Release by Binding to the Chemokine Receptor CXCR3

et al. 2008

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“…No significant expansions of the CD3 þ CD8À subset, representing gamma-delta T cells or a rare subset of CD8-alphabeta T cells, 45 were seen in any of the biopsies in our study. Gamma-delta T cells are often expanded in biopsies from patients with active celiac disease, 46 autoimmune diseases, 47 and primary B-cell immunodeficiency diseases. 55 The source of duodenal intraepithelial lymphocytes in H. pylori gastritis is not known.…”

Section: Discussionmentioning

confidence: 99%

Duodenal intraepithelial lymphocytosis with normal villous architecture: common occurrence in H. pylori gastritis

et al. 2005

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We have observed expansions of intraepithelial lymphocytes in duodenal biopsies from patients with Helicobacter pylori gastritis. This study was undertaken to prospectively evaluate, unselected, paired gastric and duodenal biopsies from 50 patients with H. pylori gastritis and a comparison group of 30 patients with other types of gastritis (10 autoimmune and 20 reactive) to: (1) quantify duodenal intraepithelial lymphocytes, determine their distribution patterns, epithelial location, and phenotype, and (2) correlate the intraepithelial lymphocyte elevations with various features of gastric and duodenal pathology. Intraepithelial lymphocytes were analyzed with antibodies including CD3, CD8, and TIA-1. A stain for H. pylori was performed on all gastric and duodenal biopsies. Duodenal intraepithelial lymphocytes from patients with H. pylori gastritis (using CD3) ranged from 3 to 42 lymphocytes/100 epithelial cells (mean 18.5) compared to 3 to 18 lymphocytes/100 epithelial cells (mean 6.6) in the comparison group. Intraepithelial lymphocyte elevations were seen in 44% of the duodenal biopsies from patients with H. pylori gastritis (using CD3). Significant differences in the intraepithelial lymphocyte counts between patients with H. pylori gastritis and the comparison group were seen for all three T-cell antigens (Po0.001 for CD3 and CD8 and Po0.002 for TIA-1). Duodenal intraepithelial lymphocytes in the H. pylori þ cases had a latent cytotoxic phenotype, H. pylori was not visualized in any of the duodenal biopsies from patients with H. pylori gastritis, and no patient had clinical evidence of celiac disease. Our study highlights frequent duodenal intraepithelial lymphocytosis in individuals with H. pylori gastritis and the lymphocyte distribution patterns (and numbers) overlapped with those described for celiac disease patients. H. pylori gastritis must be considered as a possible explanation for duodenal intraepithelial lymphocytosis with normal villous architecture, especially when lymphocytosis is patchy, intraepithelial lymphocytes display a 'latent' cytotoxic phenotype, and the clinical findings and serologic profile does not fit celiac disease.

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“…The mucosal CD3+ IELs were stained w i t h m o n o c l o n a l a n t i b o d y L e u -4 ( B e c t o n D i c k i n s o n , S a n J o s e , C A , U S A ) a n d T -c e l l receptor-γ antibody (Endogen, Woburn, MA, USA) was used to stain γδ+ IELs. A 100x flat field light microscope objective was used to count positive IELs and counted cells were expressed as cells/mm of epithelium (25). Celiac disease-specific mucosal TG2-targeted autoantibody deposits (IgA deposits) were measured by direct immunofluorescence from the frozen specimens as previously described (26,27).…”

Section: Small-bowel Mucosal Histology and Iga Depositsmentioning

confidence: 99%

Anemia and Iron Deficiency in Children With Potential Celiac Disease

Repo

Lindfors

Mäki

et al. 2017

J. pediatr. gastroenterol. nutr.

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contributed the conception and design of the work and revised the text for important intellectual content. All authors approved the final version to be published and agreed to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. AbstractObjectives: Active screening for celiac disease frequently detects seropositive children with normal villous morphology (potential celiac disease). It remains unclear whether these subjects should be treated. We here investigated the prevalence of anemia and iron deficiency in children with potential and mucosal atrophy celiac disease.Methods: The prospective study involved 19 children with potential disease, 67 with partial or subtotal villous atrophy (P/SVA) and 16 with total villous atrophy (TVA). Twenty-three healthy children comprised the control group. The groups were compared for various clinical, histological and laboratory parameters and hepcidin.Results: The prevalence of abnormal parameters was as follows (controls, potential celiac disease, P/SVA and TVA, respectively): anemia 0%, 15%, 22% and 63%; low iron 5%, 0%, 14% and 50%; increased transferrin receptor 1 (TfR1) 5%, 16%, 20% and 47%; low ferritin 0%, 21%, 35% and 87%; and low transferrin saturation 10%, 11%, 41% and 71%. One subject had low folate and none had low vitamin B12. The median values for hemoglobin, total iron, ferritin and transferrin saturation were significantly lower and TfR1 values higher in TVA group compared with other groups. After a median of seven months on a gluten-free diet hemoglobin, total iron, ferritin and albumin in children with P/SVA exceeded the baseline values in the potential celiac disease group.Conclusions: The development of anemia and iron deficiency in celiac disease is a continuum and may already be present in children with normal villous morphology, advocating an early diagnosis and possible dietary treatment of these patients.

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Intraepithelial Lymphocytes in Celiac Disease

Abstract: Counting of IELs is recommended in borderline cases where the histology is difficult to interpret. An increase especially in gammadelta+ cells strengthens the probability of CD. However, IELs are not invariably increased in CD.

Cited by 129 publications

References 25 publications

Gliadin Induces an Increase in Intestinal Permeability and Zonulin Release by Binding to the Chemokine Receptor CXCR3

Gliadin Induces an Increase in Intestinal Permeability and Zonulin Release by Binding to the Chemokine Receptor CXCR3

Duodenal intraepithelial lymphocytosis with normal villous architecture: common occurrence in H. pylori gastritis

Anemia and Iron Deficiency in Children With Potential Celiac Disease

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