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Found 4 results

  1. Celiac.com 06/20/2014 - Celiac disease is a T cell–mediated disease triggered by the protein in wheat gluten. More than 9 out of 10 of people with celiac disease carry human leukocyte antigen (HLA)-DQ2 locus. A team of researchers recently set out to determine if T-cell receptor recognition of HLA-DQ2–gliadin complexes was connected with celiac disease. The researchers included Jan Petersen, Veronica Montserrat, Jorge R Mujico, Khai Lee Loh, Dennis X Beringer, Menno van Lummel, Allan Thompson, M Luisa Mearin, Joachim Schweizer, Yvonne Kooy-Winkelaar, Jeroen van Bergen, Jan W Drijfhout, Wan-Ting Kan, Nicole L La Gruta, Robert P Anderson, Hugh H Reid, Frits Koning, and Jamie Ross. They are variously affiliated with the Department of Biochemistry and Molecular Biology at the School of Biomedical Sciences, and the Australian Research Council Centre of Excellence in Advanced Molecular Imaging at Monash University in Clayton, Victoria, Australia, the Department of Pediatrics, and the Department of Immunohematology and Blood Transfusion at Leiden University Medical Center in Leiden, The Netherlands, the Department of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, at the University of Melbourne in Parkville, Victoria, Australia, ImmusanT, Inc., in Cambridge, Massachusetts, USA, and the Institute of Infection and Immunity at Cardiff University School of Medicine in Heath Park, Cardiff, UK. The team first determined T-cell receptor (TCR) usage and fine specificity of patient-derived T-cell clones specific for two epitopes from wheat gliadin, DQ2.5-glia-α1a and DQ2.5-glia-α2. They also determined the ternary structures of four distinct biased TCRs specific for those epitopes. They were able to establish a basis for the biased TCR usage through mutagenesis and affinity measurements, together with the fact that all three TCRs specific for DQ2.5-glia-α2 docked centrally above HLA-DQ2. They found that a non–germline–encoded arginine residue within the CDR3β loop served as key of this common docking footprint. Although the TCRs specific for DQ2.5-glia-α1a and DQ2.5-glia-α2 docked similarly, their interactions with the respective gliadin determinants differed markedly, thereby providing a basis for epitope specificity. This is the first time a research team has determined that T-cell receptor recognition of HLA-DQ2–gliadin complexes was connected with celiac disease. Further study is needed to better understand the nature of their relationship. Source: NATURE STRUCTURAL & MOLECULAR BIOLOGY
  2. Celiac.com 11/22/2009 - Celiac disease has been associated with numerous other auto-immune disorders. Recently, there appeared the case of a 40-yr-old competitive strongman with celiac disease, who responded to a gluten-free diet, but developed profound and generalized motor weakness with acetylcholine receptor antibody positive myasthenia gravis, a disorder reported to occur in about 1 in 5000 people. A team of researchers set out to further explore this possible relationship between myasthenia gravis and celiac disease via serological study. The research team was made up of Hugh J Freeman, Helen R Gillett, Peter M Gillett, Joel Oger of the Department of Medicine (Gastroenterology and Neurology) at Canada's University of British Columbia. The researchers performed celiac disease screens on frozen stored serum samples from 23 acetylcholine receptor antibody positive myasthenia gravis patients with no intestinal symptoms. They examined both endomysial and tissue transglutaminase antibodies. One in 23 samples (or, about 4.3%) tested positive for both IgA-endomysial and IgA tissue transglutaminase antibodies. Subsequent endoscopic study showed duodenal mucosal scalloping, while biopsies confirmed the histopathological changes of celiac disease. From this, they concluded that celiac disease and myasthenia gravis may occur together more often than is currently understood. Muscle weakness in celiac disease may be a sign of possible occult myasthenia gravis, even in the absence of intestinal symptoms. Source: World J Gastroenterol 2009 October 14; 15(38): 4741-4744
  3. Celiac.com 04/24/2013 - Doctors classify refractory celiac disease (RCD) depending on the presence or absence of monoclonal expansions of intraepithelial lymphocytes (IELs) with an aberrant immunophenotype. A team of researchers recently set out to determine whether IEL parameters have any connection with mortality and morbidity in cases of refractory celiac disease. The research team included C. Arguelles-Grande, P. Brar, P. H. Green, and G. Bhagat. They are variously affiliated with the Celiac Disease Center, and the Departments of Medicine, Pathology and Cell Biology, at Columbia University Medical Center in New York, NY. The team used immunohistochemistry to assess IEL phenotype and polymerase chain reaction to determine T-cell receptor (TCR) gene rearrangement in 67 patients with RCD type I, and six patients with RCD type II. They considered a monoclonal TCR gene rearrangement and presence of greater than 50% CD3 CD8 IELs to be abnormal. They used Kaplan-Meier and Cox proportional hazard analyses to determine the time to worsening of clinical symptoms and the predictors of worsening. The team found 30 patients with less than 50% CD3 CD8 IELs, and eight with monoclonal TCR rearrangements. Three patients died and 40 suffered clinical worsening despite treatment. Estimated 5-year survival rates were 100% in patients with greater than 50% CD3 CD8 IELs and polyclonal TCR, but just 88% in patients with less than 50% CD3 CD8 IELs and 50% in patients with monoclonal TCR. All patients with monoclonal TCR gene rearrangement with less than 50% CD3 CD8 IELs showed shorter average time to clinical worsening of symptoms (11 mo), when compared to patients with less than 50% CD3 CD8 IELs alone (21 mo), polyclonal TCR (38 mo), or greater than 50% CD3 CD8 IELs alone (66 mo). After the team adjusted for age and gender, they found that the presence of less than 50% CD3 CD8 IELs was the only factor associated with increased risk for clinical worsening, despite negative celiac blood screens (hazard ratio=4.879; 95% confidence interval, 1.785-13.336; P=0.002). This means that RCD patients with <50% CD3 CD8 IELs are at risk for clinical worsening, and that RCD patients who also show monoclonal TCR gene rearrangement have higher mortality rates. Overall, the assessment of IEL phenotype and TCR gene rearrangement can provide important information regarding morbidity and risk of death in cases of RCD. Source: J Clin Gastroenterol. 2013 Mar 6.
  4. Celiac.com 03/26/2008 - One of the peculiarities of celiac disease is that not all gliadin proteins (peptides) are equal in terms of creating an adverse immune response. Certain peptides are completely broken down during intestinal transport, notably those that are the same size or larger than peptide 57-68. Other peptides, like the peptides 31-49 (P31-41), and the 3-mer gliadin peptide, are transported across the intestinal barrier intact and end up provoking the adverse immune response that is characteristic of celiac disease. The mechanism by which these peptides move without being broken down has remained unknown. It now looks like scientists have isolated a culprit in the transport of gliadin peptides (in the form of intact gluten particles) across the intestinal barrier. In people who can tolerate wheat well, gluten is completely broken down, or at least broken down to the point where it won’t provoke an adverse reaction from the person’s immune system. In celiac disease, it seems that certain types of gliadin proteins, notably peptide 31-49 (P31-41), trigger an adverse innate immune response. P31-41 is common to the N-terminus of the A-gliadins and is known to be toxic to people with celiac disease. The movement of intact gluten particles, particularly peptide 31-49 (P31-41) and the 33-mer gliadin, across the gut barrier is a trigger for the abnormal immune response in celiacs. Until now, the exact mechanism responsible for the movement of undigested gliadin particles across the intestinal barrier remained unknown. The research team showed that a particular receptor, the transferrin receptor CD71 is responsible for the movement of intact gliadin fragments/peptides across the intestinal barrier. The team of researchers was made up of Tamara Matysiak-Budnik, Ivan Cruz Moura, Michelle Arcos-Fajardo, Corinne Lebreton, Sandrine Ménard, Céline Candalh, Karima Ben-Khalifa , Christophe Dugave, Houda Tamouza, Guillaume van Niel, Yoram Bouhnik, Dominique Lamarque, Stanislas Chaussade, Georgia Malamut, Christophe Cellier, Nadine Cerf-Bensussan, Renato C. Monteiro, and Martine Heyman. The team undertook the study to help them better understand how undigested gluten is able to migrate across the gut barrier. The size of the study was 53 individuals. The study group looked at 26 patients with active celiac disease, 13 patients who had been following a gluten-free diet for at least 12 months, 4 patients with refractory celiac sprue, and 10 people who were free of celiac disease. In determining eligibility for the study, the standard for diagnosis of celiac disease was villous atrophy and positive serum tests for anti-gliadin, anti-Tgase, and endomysium IgA antibodies. The standard for refractory celiac sprue was resistance to a gluten-free diet, and persistence of villous atrophy when anti-gliadin IgA anti-bodies were not present. All control subjects were given a routine endoscopy, during which 4-6 consensual biopsy samples were taken, and determined to be free of celiac disease. Even in people with celiac disease, larger gliadin peptides, like the p57-68 are completely broken down before being transported across the intestinal barrier. Smaller peptides like the like the peptides 31-49 (P31-41), and the 3-mer gliadin peptide, manage to cross the intestinal barrier intact. Immuno-fluorescence studies revealed that patients with active celiac disease showed greater amounts of IgA at the apical pole of the surface epithelium, while control group and patients with treated celiac disease showed that IgA was isolated in the crypts, and did not appear in the villous epithelium. In people with active celiac disease, CD71 gets over-expressed on the apical pole, while on treated celiacs on a gluten-free diet show normal CD71 expression. For folks with refractory sprue, CD71 gets over-expressed in those individuals with flattened over-proliferation mucosa. The high rates of binding at the apical surface of enterocytes in patients with active celiac disease indicate that the transferrin receptor CD71 plays a significant role in celiac disease. JEM VOL. 205, January 21, 2008
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