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Showing results for tags 'gene'.
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Can Researchers Use Gene-Editing to Make Gluten-Safe Wheat?
Jefferson Adams posted an article in Latest Research
Celiac.com 02/11/2019 - Researchers have shown that CRISPR-Cas9 gene-editing technology can be used to remove epitopes from gliadin protein in gluten. These molecules trigger the adverse immune response seen in people with celiac disease. However, will Europe’s strict GM rules prevent this discovery from being used to create new gluten-free products for people with celiac disease? Researchers at Wageningen University in the Netherlands, and at the National Institute of Agricultural Botany (NIAB) in the UK, have shown that CRISPR-Cas9 gene-editing technology can be used to remove epitopes from gliadin protein in gluten. Gluten contains an assortment glutenin and gliadin proteins. Most of these gliadins and many of the glutenins contain immunogenic epitopes that trigger an immune response in celiacs, but others do not trigger such a reaction. As part of her PhD thesis, scientific researcher, Aurlie Jouanin, has shown that CRISPR-Cas9 gene editing technology can be used to remove certain epitopes that trigger celiac reactions. The research team did not remove all gliadin proteins from their wheat samples, which means that the wheat plants in this case were not safe for celiacs, but Jouanin found a way to spot both the genes that changed, and the ones that still required modification. Jouanin’s research suggest that it’s possible to remove just the gliadin epitopes that can trigger celiac disease. If just the offending epitopes can be removed, or altered, then the gluten proteins will not trigger the adverse immune response common in people with celiac disease, then it would be possible to make all kinds of products containing this safe gluten. Moreover, by allowing select, non-offending gliadins to remain in the bread, the result would likely be bread that is both safe for celiacs to eat, and which also has improved characteristics that are associated with traditional non-gluten-free bread. The result could be a win-win for people with celiac disease who are looking for improved gluten-free and gluten-safe great products. According to Bianca Rootsaert, director of the Dutch Coeliac Association, “gluten-free wheat would be a great improvement in the quality of life of celiac patients.” What do you think? Would you be excited to try products made from wheat that had been treated to remove celiac-triggering gluten proteins? Share your thought below. -
Celiac.com 10/15/2019 - The Good Place star Kristen Bell got some bad news earlier this year when her doctor revealed that she has a genetic marker for celiac disease. She had already started an elimination diet to clear gluten from her system and suss out other problematic food groups, when she got the word. "I was like come again? All I eat is bagels," Bell tells Women's Health. Bell said she needs carbs, "because I have to memorize 11 pages of dialogue a day...I can’t do that eating spinach and chicken." That's why even a glimmer of possible celiac disease, "...made me really nervous," she says. Still, nervousness aside, Bell seems to be taking the news in stride. Her husband, Dax Shepard, suffers from psoriatic arthritis, another autoimmune disease, that is known to improve on a gluten-free diet. Of her husband, Bell says that he's not good at keeping up with a gluten-free diet. However, the two of them might just benefit from her diagnosis with a strengthened resolve. "Who knows what that means yet but I am experimenting with being completely gluten-free, which is very annoying to do, but I think it is going to help my eczema." That's the spirit! It's good to see people meet the hard reality of a celiac diagnosis with a resolve to get the most out of it. A gluten-free diet can be tough, but the rewards for people with celiac disease are massive. Kudos to Kristen Bell for her positive outlook!
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Genetic Risk for Autoimmune Disease Tied to Gut Microbiome
Jefferson Adams posted an article in Latest Research
Celiac.com 09/04/2019 - Class II human leukocyte antigen (HLA) allele combinations exert strong genetic control over susceptibility to numerous autoimmune diseases. Researchers know that these genes are the most significant risk factors for Type 1 diabetes and celiac disease, but they still know very little about how HLA influences the makeup of the human gut microbiome, which could be an environmental factor for disease susceptibility. A team of researchers recently compared the gut microbiomes of kids with high genetic risk for Type 1 diabetes against those of kids with low genetic risk. Their results show that the two groups have very different gut microbiomes. The research team included Jordan T. Russell, Luiz F. W. Roesch, Malin Ördberg, Jorma Ilonen, Mark A. Atkinson, Desmond A. Schatz, Eric W. Triplett and Johnny Ludvigsson. Using data from a study of All Babies in Southeast Sweden, the team found that genetic risk for the development of Type 1 diabetes autoimmunity is associated with clear changes in the gut microbiome, with both core microbiome and beta diversity differing according to HLA risk group and genotype. Interestingly, protective HLA haplotypes are connected with bacterial genera Intestinibacter and Romboutsia. These results show that general population cohorts can help researchers spot potential environmental triggers or protective factors for autoimmune diseases that can otherwise remain obscured by strong genetic influence. Certain bacterial species were totally absent in children with high genetic risk, but present in children with low or no risk. "[T]his could mean that certain species [of gut bacteria] have protective effects and may be useful in future treatment to prevent autoimmune diseases. It may be that certain species cannot survive in individuals with high genetic risk”, says Johnny Ludvigsson, senior professor in the Department of Clinical and Experimental Medicine, Linköping University, and senior consultant at HRH Crown Princess Victoria Children’s Hospital, Linköping University Hospital. Read more in Nature Communications volume 10, Article number: 3621 (2019) The researchers in this study are variously affiliated with the Department of Microbiology and Cell Science, Institute of Food and Agricultural Sciences University of Florida, Gainesville, FL, USA; the Biological Sciences, Universidade Federal do Pampa, São Gabriel, Brazil; the Crown Princess Victoria Children’s Hospital, Region Östergötland, Division of Pediatrics, Linköping University, Linköping, Sweden; the Immunogenetics Laboratory, Institute of Biomedicine, University of Turku, and Clinical Microbiology, Turku University Hospital, Turku, Finland; the Department of Pathology, University of Florida Diabetes Institute, Gainesville, FL, USA; the Department of Pediatrics, College of Medicine, University of Florida, Gainesville, FL, USA; and the Department of Microbiology and Cell Science, Institute of Food and Agricultural Sciences University of Florida, Gainesville, FL, USA.-
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Celiac.com 09/05/2018 - About one out of every twenty celiac patients fails to respond to a gluten-free diet, and goes on to develop refractory celiac disease (RCD). RCD is a serious condition marked by appearance of intraepithelial T lymphocytes. Depending on the phenotype of the lymphocytes, people develop either RCD I or RCD II. Patients with RCD type II (RCDII) show clonal expansions of intraepithelial T lymphocytes, and face an especially poor prognosis. Just over half of these patients will die within five years of onset due to aggressive enteropathy-associated T-cell lymphoma. At this time, researchers don’t know whether genetic variations might play a role in the severe progression from celiac disease to RCDII. A team of researchers recently set out to try to get some answers. The team began by conducting the first genome-wide association study to identify the causal genes for RCDII, along with the molecular pathways at play in cases of RCDII. For their genome-wide association study, the team used 38 Dutch patients with RCDII, and replicated the 15 independent top-associated single nucleotide polymorphism (SNP) variants (P<5×10) in 56 independent French and Dutch patients with RCDII. The team found that, after replication, SNP rs2041570 on chromosome 7 was significantly associated with progression to RCDII (P=2.37×10, odds ratio=2.36), but not to celiac disease susceptibility. They also found that SNP rs2041570 risk allele A was associated with lower levels of FAM188B expression in blood and small intestinal biopsies. Stratifying RCDII biopsies by rs2041570 genotype revealed differential expression of innate immune and antibacterial genes that are expressed in Paneth cells. The team’s efforts resulted in the identification of a new SNP associated with the severe progression of celiac disease to RCDII. Their data suggest that genetic susceptibility to celiac disease might be unrelated to celiac progression to RCDII, and suggests that Paneth cells might play a role in RCDII progression. Source: Eur J Gastroenterol Hepatol. 2018 Aug;30(8):828-837. The research team included B Hrdlickova, CJ Mulder, G Malamut, B Meresse, M Platteel, Y Kamatani, I Ricaño-Ponce, RLJ van Wanrooij, MM Zorro, M Jan Bonder, J Gutierrez-Achury, C Cellier, A Zhernakova, P Nijeboer, P Galan, S Withoff, M Lathrop, G Bouma, RJ Xavier, B Jabri, NC Bensussan, C Wijmenga, and V Kumar. They are variously affiliated with the Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, the Department of Gastroenterology, VUMC, Amsterdam, The Netherlands, INSERM U1163, Imagine Institute and Paris Descartes University, the Department of Gastroeneterology, Georges Pompidou European Hospital, the Paris 13 University Sorbonne Paris Cité, UREN, Inserm (U557), Inra (U1125), Cnam, Bobigny, France, the scientific director of McGill University and Génome Québec Innovation Centre, Montréal, Québec, Canada, the Gastrointestinal Unit and Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital and Harvard Medical School, Boston, The Broad Institute of MIT and Harvard, Cambridge, Massachusetts, the Department of Medicine, University of Chicago, Chicago, Illinois, USA., and the K.G. Jebsen Coeliac Disease Research Centre, Department of Immunology, University of Oslo, Norway.
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Hi I am wondering if anyone was tested being negative for blood and or gene tests and later tested positive for Celiac. I was tested quite a few times but was already on a gluten free or very limited gluten diet. I also did the gene test which was negative and my previous GI Dr swore I could never have Celiac, but today my new nutritionist just told me that is absolutely false that is it still possible to have it. Because I have other autoimmune, HLA-B27, gastroparesis, IBS, acne (and cystic acne), eczema, and a bunch of other issues until he knows for sure he is treating me as if I have it. Help would be appreciated. Thanks
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Is it possible to have the celiac gene and be non-celiac gluten sensitive? Or if you are reacting to gluten and carry the gene, does that give an indication of celiac? My son's blood test came back negative, but the doctor wouldn't do an endo biopsy because she said he didn't have celiac. But if he carries the gene and had symptoms, wouldn't that be a red flag? Or could he carry the gene, have symptoms, and still just be NCGS?
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I would like some help in understanding my results from the 23andme test. I am being told that I have 2 copies of a genetic variant that was tested. The variants were detected in the HLA-DQA1 gene. "We detected two copies of a variant linked to the HLA-DQ2.5 haplotype." Do do these results mean? In the HLA-DQ2.5 - HLA-DQa1 - rs2187668 - there are two TT. Is this bad? Is this what is mean by having homozygous hla dqa2.5? I am new to all of this and am just looking for some answers. I am concerned about being at risk for celiac disease. Thanks!
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Can Gene Cells Reveal Extent of Celiac-Related Gut Damage?
Jefferson Adams posted an article in Latest Research
Celiac.com 06/27/2017 - What can gene cells tell us about potential gut damage in people with celiac disease? Can they be harnessed to paint an accurate picture of what's going on in the gut? A team of researchers recently set out to study autoimmunity and the transition in immune cells as dietary gluten induces small intestinal lesions. Specifically, they wanted to know if a B-cell gene signature correlates with the extent of gluten-induced gut damage in celiac disease. The research team included Mitchell E. Garber, Alok Saldanha, Joel S. Parker, Wendell D. Jones, Katri Kaukinen, Kaija Laurila, Marja-Leena Lähdeaho, Purvesh Khatri, Chaitan Khosla, Daniel C. Adelman, and Markku Mäki. They are variously affiliated with the Alvine Pharmaceuticals, Inc, San Carlos, California, the Department of Chemistry, Stanford, California, the Institute for Immunity, Transplantation and Infection, Stanford, California, the Division of Biomedical Informatics, Department of Medicine, Stanford, California, the Department of Chemical Engineering, Stanford, California, the Stanford ChEM-H, Stanford University, Stanford, California, the InterSystems Corporation, Cambridge, Massachusetts, the Lineberger Comprehensive Cancer Center, Chapel Hill, North Carolina, the Department of Genetics, University of North Carolina, Chapel Hill, North Carolina, the EA Genomics, Division of Q2 Solutions, Morrisville, North Carolina, the Tampere Center for Child Health Research, Tampere, Finland, the University of Tampere Faculty of Medicine and Life Sciences, Tampere, Finland, the Department of Pediatrics, Tampere, Finland, the Department of Internal Medicine, Tampere, Finland, Tampere University Hospital, Tampere, Finland, and with the Division of Allergy/Immunology, Department of Medicine, University of California San Francisco, San Francisco, California. The team looked at seventy-three celiac disease patients who followed a long-term, gluten-free diet. Those patients ingested a known amount of gluten daily for 6 weeks. Prior to the study, the team took a peripheral blood sample and intestinal biopsy specimens, then did the same after 6 weeks of gluten challenge. To accurately quantify gluten-induced intestinal injury, they reported biopsy results on a continuous numeric scale that measured the villus-height–to–crypt-depth ratio. As patient gut mucosa remained either relatively healthy or else deteriorated under the gluten challenge, the team isolated pooled B and T cells from whole blood, and used DNA microarray to analyze RNA for changes in peripheral B- and T-cell gene expression that correlated with changes in villus height to crypt depth. As is often the case with celiac disease, intestinal damage from the gluten challenge varied considerably among the patients, ranging from no visible damage to extensive damage. Genes differentially expressed in B cells correlated strongly with the extent of gut damage. Increased B-cell gene expression correlated with a lack of sensitivity to gluten, whereas their decrease correlated with gluten-caused mucosal damage. The the correlation with gut damage was tied to a core B-cell gene module, representing a subset of B-cell genes analyzed. In patients with little to no intestinal damage, genes comprising the core B-cell module showed an overall increase in expression over the 6 week period. This suggests that B-cell immune response in these patients may be a reaction to promote mucosal homeostasis and circumvent inflammation. The idea that B-cell gene signature can reveal the extent of gut damage in celiac patients is intriguing. Clearly more research is needed to determine how this revelation might be harnessed to improve the evaluation and treatment of celiac disease. Source: Cell Mol Gastroenterol Hepatol. 2017 Jul; 4(1): 1–17. Published online 2017 Jan 28. doi: 10.1016/j.jcmgh.2017.01.011. PMCID: PMC5413199-
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