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T lymphocyte populations within the lamina propria
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Thomas T. MacDonald, Antonio Di Sabatino
Celiac disease is of interest because there is no doubt that a substantial part of the pathology is driven by CD4 T cells in the lamina propria responding to gliadin peptides presented in the context of HLA-DQ2 or DQ8. However, DQ2 is an extremely common haplotype in the general population, and it is still not known what additional factors lead to only a few percent of DQ2+ individuals becoming gluten reactive. Environmental factors are clearly important. There are cases in the literature where identical twins have developed celiac disease years apart, and when the proband was diagnosed, the healthy sibling has been investigated thoroughly and shown to be normal. One notion is that viral infections in the gut not only break the barrier to allow antigen to enter the lamina propria but can induce the local production of type I interferons, which are potent stimulators of TH1 responses. Once sensitized, however, celiac disease is a lifelong condition, which implies T-cell memory. It is highly unlikely that long-lived gluten-specific memory T cells persist in the lamina propria; instead they are probably part of the recirculating memory T-cell pool, in which case they may encounter gluten in GALT. One feature of celiac disease, however, that has not been explained is the time to relapse when returning to a gluten-containing diet. This is highly variable between individuals and implies that environmental factors may also be important at all stages of the disease.
Lactic Acid Bacteria Application to Decrease Food Allergies
Published in Marcela Albuquerque Cavalcanti de Albuquerque, Alejandra de Moreno de LeBlanc, Jean Guy LeBlanc, Raquel Bedani, Lactic Acid Bacteria, 2020
Vanessa Biscola, Marcela Albuquerque Cavalcanti de Albuquerque, Tatiana Pacheco Nunes, Antonio Diogo Silva Vieira, Bernadette Dora Gombossy de Melo Franco
As for celiac disease (CD), it is a chronic inflammatory enteropathy that affects the small intestine and occurs when genetically predisposed individuals are exposed to gluten, which compromises the integrity of their intestinal epithelium (Herrán et al. 2017, Leonard et al. 2017). About 40% of humans have the HLA-DQ2 and HLA-DQ8 genotypes (present in 90% and 10% of celiac individuals, respectively). However, only 2% to 3% of these individuals develop CD. Its prevalence in the general population is about 1%, and this number can vary in different countries. In Northern Europe, North Africa, Middle East, and India, the occurrence of CD has become an increasingly common problem (Leonard et al. 2017, Watkins and Zawahir 2017).
Answers
Published in Andrew Schofield, Paul Schofield, The Complete SAQ Study Guide, 2019
Andrew Schofield, Paul Schofield
Coeliac disease is a T-cell-mediated autoimmune disease affecting the small bowel in which prolamin found in rye, barley and wheat causes loss of villous architecture, which leads to malabsorption. It is associated with HLA-DQ2 and is commoner in northern European populations. Symptoms include abdominal pain, weight loss, weakness and steator-rhoea. Iron-deficiency anaemia may also be present. Time to diagnosis may be delayed, so a high index of suspicion is important. Blood investigations include antibodies to alpha-gliadin, tissue transglutaminase and endomysial. Gold-standard diagnosis is duodenal biopsies, which reveal villous atrophy. The best treatment is complete removal of gluten from the diet, which should be maintained for life. Gluten-free food is available on prescription, and patients should be educated on the foods to avoid. Complications include T cell lymphoma, increased risk of malignancy and effects of malnutrition.
Gut inflammation in CVID: causes and consequences
Published in Expert Review of Clinical Immunology, 2022
Venhoff et al. also explored the association between the celiac disease related HLA profiles and celiac disease-like findings in duodenal biopsies in 20 patients. All patients had increased IEL and diarrhea (chronic or recurrent), and 75% had villous atrophy, whereas half of the patients had malabsorption. Only four of these (20%) carried the celiac disease related HLA profile [36], suggesting limited association between celiac disease related HLA profile and histopathological changes resembling celiac disease in symptomatic CVID patients. Likewise, in a larger cohort (n = 50), we found no correlation between the histological findings resembling celiac disease and the celiac disease related HLA profiles, HLA-DQ2 and HLA-DQ8. Furthermore, when comparing gene-expression analysis from duodenal biopsies, we found that CVID patients with ‘celiac-like disease’ and true celiac disease were different [19], suggesting that these similar histological findings represent different disease mechanisms and disease entities.
Estimation of the celiac disease prevalence in Denmark and the diagnostic value of HLA-DQ2/DQ8
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2020
Flemming Lund, Merete Frejstrup Pedersen, Søren Kristiansen
From February 2012 to March 2017, three different HLA assays were used as previously described [16]. In brief, we applied a Method 1 using six single nucleotide polymorphisms (SNP) to identify the risk variants HLA-DQ2.2, DQ2.5, DQ7, and DQ8 based on TaqMan SNP Genotyping Assays (Applied Biosystems, Foster City, CA) on a 7500 Fast Real Time PCR system (Applied Biosystems) [17]. HLA typing by SNP technique was compared with two other alternative HLA techniques, a sequence specific primer amplification (SSP) technique (Method 2) [18,19]) and a commercial HLA typing assay, Celiac Typing (BioDiagene, Palermo, Italy distributed by Thermo Fisher Scientific, Allerød, Denmark) as Method 3. From March 2017 to October 2018 a commercial HLA kit replaced the previous three methods with Method 4 (EUROArray HLA-DQ2/DQ8, EUROIMMUN, Lübeck, Germany) after a validation. All tests are designed for determination of celiac disease-associated HLA-DQA1 and HLA-DQB1 alleles which code for the alpha- and beta-subunits of the HLA-DQ2 and HLA-DQ8 molecules. Both HLA-DQ2.2 and HLA-DQ2.5 were tested and included as positive for HLA-DQ2 determination. The analyses do not distinguish between HLA-DQ2 homozygous or heterozygous individuals. The analyses were participated in the external quality program HLA diseases for Coeliac Disease provided by UK NEQAS, Pontyclun, UK.
A case of celiac disease presenting with celiac crisis: rare and life threatening presentation
Published in Journal of Community Hospital Internal Medicine Perspectives, 2019
Rakshya Poudyal, Saroj Lohani, William B. Kimmel
Celiac disease (also called gluten sensitive enteropathy and nontropical sprue) is an immune mediated disease of small intestine characterized by malabsorption symptoms and villous atrophy precipitated by gluten protein [6]. Originally considered as a rare disease of childhood it now affects people of all age groups [6]. It was first reported by Samuel Gee in 1888 [7]. Celiac disease is closely associated with HLA-DQ2 and/or DQ8 gene loci hence it is believed to be caused by immune disorder in genetically susceptible population triggered by gliadin component of gluten [8]. Celiac disease is diagnosed by serologic evaluation (anti-tissue transglutaminase (TTG) antibody, anti endomysial antibody, anti Deaminated Gliadin Peptide (DGP) antibody), genetic testing for HLA DQ2/DQ8 and small intestinal biopsy [8]. Histologic findings include intraepithelial lymphocytes, loss of villi, flat mucosa and crypt hyperplasia [9,10].