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Found 5 results

  1. Celiac.com 05/30/2016 - People with HLA genes have the highest risk factor for developing autoimmune disorders. The vast majority of people with celiac disease carry the HLA DQA1*05 and DQB1*02 alleles, both of which encode the DQ2.5 molecule. A research team recently set out to examine the implications for anti-gluten T cell response of the preferential expression of HLA-DQ2.5 genes associated with celiac disease with respect to non-predisposing HLA genes. The research team included L Pisapia, A Camarca, S Picascia, V Bassi, P Barba, G Del Pozzo, and C Gianfrani. They are variously affiliated with the Institute of Protein Biochemistry-CNR, the Institute of Genetics and Biophysics-CNR in Naples, Italy, and the Institute of Food Sciences-CNR in Avellino, Italy. In order to activate pathogenic CD4+ T lymphocytes, that is, to trigger active celiac disease, it is necessary for the body to form complexes between DQ2.5 and gluten peptides on antigen-presenting cells (APCs). It is widely accepted by clinicians that the DQ2.5 genes establish the different intensities of anti-gluten immunity, depending on whether they are in a heterozygous or a homozygous configuration, that is, whether both genes are activated, or only one gene is activated. The research team's recent study shows that, in celiac patients, HLA DQA1*05 and DQB1*02 gene expression is much higher than expression of non-celiac-associated genes. This, in turn, impacts protein levels and causes a comparable cell surface exposure of DQ2.5 heterodimers between DQ2.5 homozygous and heterozygous celiac patients. As a consequence, the magnitude of the anti-gluten CD4+ T cell response is strictly dependent on the antigen dose, and not on the DQ2.5 gene configuration of APCs. These findings are important, because they support the idea that the expression of DQ2.5 genes is an important risk factor in celiac disease. The preferential expression of DQ2.5 alleles observed in this study offers a new explanation of why these genes are so frequently associated with celiac disease and with other autoimmune disorders. Source: J Autoimmun. 2016 Apr 12. pii: S0896-8411(16)30029-4. doi: 10.1016/j.jaut.2016.03.016.
  2. Celiac.com 06/01/2010 - A clinical research team recently examined the increased expression of hypoxia inducible factor 1alpha in celiac disease. The team included A. Vannay, E. Sziksz, A. Prókai, G. Veres, K. Molnár, D. Nagy Szakál, A. Onódy, I. R. Korponay-Szabó, A. Szabó, T. Tulassay, A. Arató, and B. Szebeni. They are affiliated with the First Department of Pediatrics at Semmelweis University, and with the Department of Gastroenterology-Nephrology of Heim Pal Children's Hospital, both in Budapest, Hungary. They are also involved with the Research Group for Pediatrics and Nephrology, a joint project between the two institutions. The team set out to follow-up on the hypothesis that hypoxia inducible factor (HIF) 1 signaling may play a key role in maintaining the barrier function of the intestinal epithelium in cases of inflammatory bowel disease (IBD). In their 2008 article, "The human side of hypoxia-inducible factor," which appeared in the British Journal of Haematology, Smith, Robbins and Ratcliffe define Hypoxia-inducible factors (HIFs) as transcription factors that respond to changes in available oxygen in the cellular environment, specifically, to decreases in oxygen, or hypoxia. The team wanted to characterize the variation of HIF-1alpha and related genes in celiac disease, where the importance of the barrier function is well understood. To accomplish their goal, they gathered duodenal biopsy specimens from 16 children with untreated celiac disease, 9 children with treated celiac disease, and 10 control subjects. They assessed HIF-1alpha, trefoil factor 1 (TFF1), ecto-5-prime nucleotidase (CD73) and multi-drug resistance gene 1 (MDR1) mRNA and HIF-1alpha protein expression by real-time PCR and Western blot, respectively. They assessed localization of HIF-1alpha by immunofluorescent staining. The team observed increased HIF-1alpha and TFF1 mRNA and HIF-1alpha protein expression in the duodenal mucosa of children with untreated celiac disease compared to either the control subjects, or those with treated celiac disease (p<0.05). Children with untreated celiac disease showed HIF-1alpha staining in cytoplasmic and nuclear region of the villous enterocytes. Children with treated celiac disease showed increased mRNA expression of CD73 and MDR1 versus control subjects (p<0.01 and 0.05, respectively). The results of increased mucosal HIF-1alpha expression in children with celiac disease suggests influences from this signaling pathway in the pathological mechanisms of celiac disease. Source: Pediatr Res. 2010 May 5. PMID: 20453713
  3. Celiac.com 03/15/2010 - A team of researchers recently set out to investigate mucosal expression of claudins 2, 3 and 4 in the proximal and distal parts of duodenum in children with celiac disease. The team included Dorottya Nagy Szakál, Hajnalka GyÅ‘rffy, András Arató, Áron Cseh, Kriszta Molnár, Mária Papp, Antal DezsÅ‘fi, and Gábor Veres. They are variously associated with the Department of Pediatrics, and the Department of Pathology at Semmelweis University in Budapest, Hungary, and the Department of Medicine at the University of Debrecen in Debrecen, Hungary. Duodenal biopsy is an important tool for properly diagnosing celiac disease. However, the issue of finding the best site for taking biopsy samples that will give the best results for diagnosing celiac disease is still not fully resolved. Claudins (CLDNs), belong to a large group of related adherent junction proteins, which are known to express characteristic patterns in inflammatory disorders. However, doctors presently know nothing about CLDN expression in people with celiac disease. To address the situation, the team performed a comparative study to examine the CLDN 2, 3 and 4 expressions in both the proximal and distal parts of duodenum in children with celiac disease and in control subjects. For the study, they enrolled a total of forty-seven children. Thirty-three had newly diagnosed celiac disease, while fourteen healthy children served as control subjects. The team took biopsies from proximal and distal part of duodenum, and used immunohistochemistry to detect CD3+ intraepithelial lymphocytes and CLDN 2, 3 and 4 protein expressions. Whether taken from proximal or distal part of duodenum, biopsies revealed no differences under macroscopic imaging, routine histology and Marsh grading. However, in comparison to controls, patients with severe celiac disease showed significantly higher CLDN 2 expression in bulb and in distal duodenum, while non-severe celiac patients showed higher distal CLDN 2 expression. The data showed similar associations regarding CLDN 3 expression. All groups showed similar expression of CLDN 4. The data showed that both proximal and distal mucosal duodenal biopsies are suitable for diagnosing villous atrophy in patients with celiac disease. Finally, the team noted that increased expressions of CLDN 2 and 3 imply structural changes of tight junction in celiac disease, which may play a role in increased permeability and proliferation observed in celiac disease. Source: Virchows Archive, Volume 456, Number 3 / March, 2010
  4. Celiac.com 03/11/2010 - As part of an effort to investigate the possibility of multiple common variants for celiac disease influencing immune gene expression, a team of more than sixty scientists recently worked together to conduct a second-generation genome-wide association study (GWAS) of 4,533 individuals with clinically proven celiac disease, along with 10,750 control subjects. They genotyped a total of 113 selected SNPs with PGWAS < 10−4 and 18 SNPs from 14 known loci in another 4,918 confirmed celiac disease patients and 5,684 control subjects. The research team included dozens of scientists associated with a variety of major research institutions, hospitals and clinics. The GWAS included five European sample collections of celiac disease and control cases, including the celiac disease dataset reported previously. The team's stringent data quality control measures included calling genotypes using a custom algorithm on both large sample sets and, where possible, cases and controls together. The team tested 292,387 non-HLA SNPs from the Illumina Hap300 marker pool for association in 4,533 individuals with celiac disease and 10,750 control subjects of European descent. They also tested another 231,362 additional non-HLA markers from the Illumina Hap550 marker set for association in a subset of 3,796 individuals with celiac disease and 8,154 controls. All markers came from autosomes or the X chromosome. For both datasets, Genotype call rates were >99.9%. The study showed over-dispersion factor of association test statistics comparable to that observed in other GWASs of this sample size. Factoring in missing genotypes for 737 cases with celiac disease genotyped on the Hap300 BeadChip and corresponding controls did not change the findings in any meaningful way.Variants from 13 new regions reached genome-wide significance (Pcombined < 5 × 10−8); most contain geneswith immune functions, such as BACH2, CCR4, CD80, CIITA-SOCS1-CLEC16A, ICOSLG and ZMIZ1, while ETS1, RUNX3, THEMIS and TNFRSF14 play key roles in thymic T-cell selection. The data suggested associations for 13 additional regions. Expression quantitative trait meta-analysis of 1,469 whole blood samples showed that 52.6% of tested loci (20 of 38 loci) had celiac risk variants corresponding with cis gene expression (P < 0.0028, FDR 5%). Source: Nature Genetics (28 February 2010) | doi:10.1038/ng.543
  5. Celiac.com 10/28/2009 - Celiac disease is a T cell-mediated autoimmune disease, and a number of clinicians have described up-regulation of T-bet and phosphorylated signal transducers and activators of transcription (pSTAT)1, both of which are key transcription factors for the development of T helper type 1 (Th1) cells, in the mucosa of patients with untreated celiac disease. A team of researchers recently used transcription factor analysis to examine whether celiac patients up-regulate T-bet and pSTAT1 expressions in peripheral blood and whether such up-regulation may be associated with celiac disease activity. The research team was made up of G. Frisullo, V. Nociti, R. Iorio, A. K. Patanella, D. Plantone, A. Bianco, A. Marti, G. Cammarota, P. A. Tonali, and A. P. Batocchi of the Department of Neurosciences at the Catholic University in Rome, Italy. The team used flow cytometry to analyze T-bet, pSTAT1 and pSTAT3 expression in CD4(+), CD8(+) T cells, CD19(+) B cells and monocytes from peripheral blood of 15 untreated and 15 treated celiac disease patients and 30 controls, and longitudinally in five celiac patients before and after dietary treatment. The team measured the results using enzyme-linked immunosorbent assay (ELISA), interferon (FN)-gamma, interleukin (IL)-17 and IL-10 production by peripheral blood mononuclear cell (PBMC) cultures. Patients with untreated celiac disease showed higher T-bet expression in CD4(+), CD8(+) T cells, CD19(+) B cells and monocytes and IFN-gamma production by PBMC, than either treated celiac patients or control subjects. CD4(+)T cells, B cells and monocytes from untreated celiac patients showed higher pSTAT1 expression than either treated celiac patients or controls. Only in monocytes from untreated patients showed increased pSTAT3 compared with treated celiac patients and controls. Data from longitudinal evaluation of transcription factors corroborated these findings. Flow cytometric analysis of pSTAT1 and T-bet protein expression in peripheral blood mononuclear cells could be useful and sensible markers in the follow-up of celiac disease patients to evaluate disease activity and response to dietary treatment. Being able to spot celiac disease early is key to achieving optimal outcomes for celiac patients. The development of simple, reliable, low-cost tests is key to that effort. Stay tuned for more developments regarding celiac disease testing, screening and diagnosis. Source: Clinical & Experimental Immunology, Volume 158 Issue 1, Pages 106 - 114