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Found 7 results

  1. Celiac.com 08/29/2018 - Up to one in twelve patients with gluten sensitivity develops neurological symptoms such as ataxia, dementia, seizures or peripheral neuropathy, though the reasons for this are still poorly understood. As a means of better understanding the immunological mechanisms behind this reality, a team of researchers recently reported the case of a 68‐year‐old male patient suffering from progressive ataxia and dementia associated with chronic diarrhea, and both elevated IgG and IgA antigliadin‐antibodies. The research team included Michel Mittelbronn, Jens Schittenhelm, Gellert Bakos, Rob A. De Vos, Manfred Wehrmann, Richard Meyermann, and Katrin Bürk. They are variously affiliated with the Institute of Brain Research at the University of Tübingen, and the Institute for Cell Biology, Department of Immunology at the University of Tübingen, Tübingen, Germany, the Neurological Institute/Edinger Institute, Goethe University Medical School, Frankfurt, the Department of Pathology, St. Georg Hospital, Leipzig, Germany, and with the Laboratory for Pathology, Enschede, the Netherlands. Autopsy indicated that frequent argyrophilic glial and neuronal inclusions within the basal nucleus of Meynert were the structural markers of the cognitive decline. The patient showed substantial neuronal loss in the cerebellar cortex and the inferior olives, along with infiltrating CD8+/perforin+/granzyme B+ cells, and reactive astrogliosis and microglial activation. In patients with gluten sensitivity and neurological disease, it is likely that CD8+ cytotoxic T and NK cells function as effector cells that trigger neuronal cell death, and thus might play some role in triggering cerebellar symptoms in gluten ataxia cases. The team concludes by noting that an absence of B‐ or plasma cells, along with multiple CD8+, granzyme B and perforin expressing cells in ataxia‐associated brain areas, indicates pronounced cytotoxic effects in neuro-pathogenesis of gluten sensitivity. This is one of the first reports to indicate that CD8+, perforin+, and granzyme B+ effector cells infiltrate the cerebellum and inferior olives in cases of gluten ataxia. Read more in: Neuropathology
  2. Celiac.com 12/22/2016 - The nature of gut intraepithelial lymphocytes (IELs) lacking antigen receptors remains controversial. A team of researchers recently set out to better understand the mechanisms by which innate intraepithelial lymphocytes develop in the intestine and become cancerous in celiac disease patients. The research team included J Ettersperger, N Montcuquet, G Malamut, N Guegan, S Lopez-Lastra, S Gayraud, C Reimann, E Vidal, N Cagnard, P Villarese, I Andre-Schmutz, R Gomes Domingues, C Godinho-Silva, H Veiga-Fernandes, L Lhermitte, V Asnafi, E Macintyre, C Cellier, K Beldjord, JP Di Santo, N Cerf-Bensussan, and B Meresse. They are variously affiliated with the INSERM UMR1163, Laboratory of Intestinal Immunity, Institut Imagine; Laboratory of Human Lymphohematopoiesis; Institut Necker-Enfants-Malades, INSERM UMR1151 and, Biological Hematology, AP-HP Necker-Enfants-Malades; the Université Paris Descartes-Sorbonne Paris Cité and Institut Imagine in Paris, France; AP-HP, Department of Gastroenterology, Hôpital Européen Georges Pompidou, 75015 Paris, France; Institut Universitaire d'Hématologie, Hôpital Saint-Louis, Paris, France; Innate Immunity Unit, Institut Pasteur, 75015 Paris, France; INSERM U 668, Paris, France; Paris-Descartes Bioinformatic Platform, 75015 Paris, France; and with the Instituto de Medicina Molecular, Faculdade de Medicina de Lisboa in Lisbon, Portugal. The team was able to show, in humans and in mice, innate intestinal IELs expressing intracellular CD3 (iCD3(+)) differentiate along an Id2 transcription factor (TF)-independent pathway in response to TF NOTCH1, interleukin-15 (IL-15), and Granzyme B signals. In NOTCH1-activated human hematopoietic precursors, IL-15 induced Granzyme B, which cleaved NOTCH1 into a peptide lacking transcriptional activity. As a result, NOTCH1 target genes necessary for T cell differentiation were silenced, and precursors were reprogrammed into innate cells with T cell marks, including intracellular CD3 and T cell rearrangements. In the intraepithelial lymphoma complicating celiac disease, iCD3(+) innate IELs acquired gain-of-function mutations in Janus kinase 1 or Signal transducer and activator of transcription 3, which enhanced their response to IL-15. The research team observed and described gut T cell-like innate IELs, decoded their pathway of change, and showed their malignant transformation in celiac disease. This study offers an exciting glimpse into the hard work being done in the far corners of celiac disease and cancer research. Source: Immunity. 2016 Sep 20;45(3):610-25. doi: 10.1016/j.immuni.2016.07.018. Epub 2016 Sep 6.
  3. I've been experiencing some Celiac-like symptoms for a while now and could use some help making sense of these test results. Some history: I had a partial thyroidectomy 13 years ago (benign Follicular Adenoma). I take Synthroid 112 mcg daily. About 3 years ago, I starting experiencing hair loss, which my doctor attributed this to my throid and increased my synthroid. Then, I starting having numbness in my feet. My endo was concerned and ran what seemed like a million tests to discover that I was Vitamin B12 deficient. She told me to take OTC megadoses and then retested me to find I was still deficient. She prescribed B12 injections. The B12 seems to have stabilized, but still isn't ideal. Then, she tested my Vitamin D and found I was severally deficient there. OTC prescribed with no improvement. Prescription Vitamin D (50,000 Iu) every 7 days and then retested. I was still deficient and now my calcium was dangerously low, probably due to low D. Continued with the Vitamin D megadoses and then retested-both D and Calcium dangerously low and now my TSH is out of whack. The endo had me increase the D to 50,000 Iu every 5 days and add 600 mg of Calcium every night. She said she won't increase my Synthroid because she doesn't think I'm absorbing it and then referred me to a GI. I meet with the Gi who asks me about other symptoms. I report heartburn, flipping between consitpation and diarrhea, gas and bloating...He orders the blood test below and schedules an EGD. Immunoglobulin A, Qn, Serum 87 mg/dL (70-400) Deamidated Gliadin Abs, IgA 2 units (0-19) Negative 0 - 19 Weak Positive 20 - 30 Moderate to Strong Positive >30 Deamidated Gliadin Abs, IgG 3 units (0-19) Negative 0 - 19 Weak Positive 20 - 30 Moderate to Strong Positive >30 t-Transglutaminase (tTG) IgA <2 U/mL (0-3) Negative 0 - 3 Weak Positive 4 - 10 Positive >10 t-Transglutaminase (tTG) IgG <2 U/mL (0-5) Negative 0 - 5 Weak Positive 6 - 9 Positive >9 Endomysial IgA Negative After the EGD, the GI tells me that I have esophagitis and a gastric ulcer. They pulled tissue samples for a biopsy. He started me on a PPI to heal the ulcer. I heard from the nurse practitioner today, my biopsy results show lympohcytes indicative of early Celiac Disease but I have negative blood tests. I return to the doctor this Wednesday. Does anyone have any idea what this means?
  4. Celiac.com 10/25/2012 - Abnormal intraepithelial lymphocytes (IELs) are the main feature of refractory celiac disease type II (RCDII). However, researchers still don't know exactly how these abnormal IELs originate. A pair of researchers recently commented on efforts to learn how these abnormal IELs might come about. The pair were Victor F. Zevallos, and Detlef Schuppan, of the center for Molecular and Translational Medicine, Department of Medicine I at the University Medical Center of Johannes Gutenberg University Mainz, in Mainz, Germany. Their commentary focuses on efforts by a separate research team, Schmitz, et al., which had already used a broad spectrum of cell specific markers, RNA array and immunological techniques, to explore abnormal IEL cell lines from four RCDII patients, and compare them with IELs from the fetal intestine, the intestine of children and adults and the thymus. IELs are highly varied lymphocytes cells with innate and adaptive features that live in the small and large intestine. IELs play an important role in maintaining gut tolerance to common food antigens versus defense against pathogens. A number of nutritional factors influence the development and spread of IELs, especially vitamins and their active metabolites, such as retinoic acid, and phytochemicals such as ligands of the aryl hydrocarbon receptor from cruciferous vegetables. However, when IELs activate and expand uncontrollably in response to chronic inflammatory conditions in the gut, they trigger mucosal damage, which can lead to celiac disease, and in some cases, to malignant cancers. Up to 5% of people with celiac disease, especially those who are over fifty years old when diagnosed, continue to suffer from clinical symptoms and villous atrophy even when following a gluten-free diet. After excluding ongoing gluten consumption and other potential underlying diseases, all four patients studied by Schmitz could be diagnosed with RCD, which is classically classified as type I or type II, based on the histological co-expression of CD3 and CD8 in RCDI, or absence of such co-expression in RCDII. Read the entire report in Gut. Source: Gut doi:10.1136/gutjnl-2012-303030
  5. Celiac.com 05/19/2010 - Enteropathy-associated T cell lymphoma is a serious complication of celiac disease, and a major cause of mortality in untreated celiac disease. One possible trigger for Enteropathy-associated T cell lymphoma development is chronic exposure of intraepithelial lymphocytes (IELs) to strong anti-apoptotic signals, that is, signals that interfere in the normal mortality of the IEL cells. These signals are triggered by IL-15, a cytokine that is over-expressed in the enterocytes of people with celiac disease. However, researchers have not yet fully mapped the signaling pathway by which IL-15 transmits these anti-apoptotic signals. Researchers consider type II refractory celiac disease (RCDII) to be a middle step between celiac disease and enteropathy-associated T cell lymphoma. Eliminating abnormal IELs at the RCDII stage would likely block EATL development. So far, though, scientists have not found successful immunosuppressive and/or chemotherapeutic approaches able to accomplish this, and RCDII outcomes remain very poor. A team of researchers recently set out to map the IL-15–driven survival pathway in human IELs, and to determine whether IL-15 triggered pathway in human intraepithelial lymphocytes represents a possible new target in type II refractory celiac disease and enteropathy-associated T cell lymphoma. The research team was made up of Georgia Malamut, Raja El Machhour, Nicolas Montcuquet, Séverine Martin-Lannerée, Isabelle Dusanter-Fourt, Virginie Verkarre, Jean-Jacques Mention, Gabriel Rahmi, Hiroshi Kiyono, Eric A. Butz, Nicole Brousse, Christophe Cellier, Nadine Cerf-Bensussan, and Bertrand Meresse. The are variously affiliated with INSERM U989, the Université Paris Descartes, Faculté de Médecine René Descartes, the Department of Gastroenterology, AP-HP, Hôpital Européen Georges Pompidou, the Institut Cochin, Université Paris Descartes, CNRS (UMR 8104), INSERM U1016, the Department of Pathology, AP-HP, of the Hôpital Necker-Enfants Malades in Paris, with the Division of Mucosal Immunology, Department of Microbiology and Immunology at the Institute of Medical Science at the University of Tokyo in Japan, and the Inflammation Department of AMGEN Inc., in Seattle, Washington, USA. Their current findings reveal that the survival signals IL-15 directs to freshly isolated human IELs, and to human IEL cell lines derived from celiac disease patients with type II refractory celiac disease, depend on anti-apoptotic factors Bcl-2 and/or Bcl-xL. The signals require IL-15Rβ, Jak3, and STAT5 for proper function, but functioned independently of PI3K, ERK, and STAT3. In support of these findings, the team recorded elevated levels of Bcl-xL, phospho-Jak3, and phospho-STAT5 in IELs from patients with active celiac disease and RCDII. Moreover, by incubating patient duodenal biopsies with a fully humanized human IL-15–specific Ab, the team effectively blocked Jak3 and STAT5 phosphorylation. Also, treatment with IL-15–specific Ab caused IEL cell mortality, and wiped out the massive IEL build-up in mice over-expressing human IL-15 in their gut epithelium. The study marks the first successful mapping of the IL-15–driven survival pathway in human IELs, and demonstrates that IL-15 and its downstream effectors are meaningful therapeutic targets in RCDII. These findings will likely help to pave the way for the development of successful immunosuppressive and/or chemotherapeutic treatments that destroy abnormal IELs at the RCDII stage and help to block EATL development, improving outcomes for RCDII patients. Source: Journal of Clinical Investigation doi:10.1172/JCI41344
  6. Celiac.com 08/29/2007 - A study that appeared in the August issue of Journal of Clinical Gastroenterology, found that celiac disease and small intestinal bacterial growth both show increased levels of intraepithelial lymphocytes (IELs), especially gammadelta+ IELs. A sharp increase in gammadelta+ IELs has been noted in people with celiac disease, but little is known about the role of this particular class of IELs in other intestinal pathologies. A team of researchers led by J.M. Remes-Troche set out to assess the levels of IEls, especially of gammadelta+, in the duodenal mucosa biopsies from individuals w/ celiac disease and to compare them with those of patients with small intestinal bacterial overgrowth (SIBO), and irritable bowel syndrome (IBS). The study team looked at 12 individuals with untreated celiac disease, 8 patients with SIBO, and 10 patients with diarrhea-predominant IBS. All patients were given an upper-endoscopy for mucosal biopsy and jejunal aspirate. Intraepithelial cells were isolated from 2 small bowel biopsies, and labeled with monoclonal antibodies CD103-PE (phycoerythrin), CD3-FITC (fluoresecein isothio-cynate), celiac disease-7R-PE, CD45RO-APC (allophycocyanin), and TcR gammadelta-FITC. Researchers conducted flow cytometry analysis using a standard FACScan. Total IEL levels and subsequent levels were catalogued as percentages as follows: 16.7 +/- 6% for IBS patients; 25.7 +/- 17% for SIBO patients; and 26 +/- +/- 13% in celiac patients (P=0.2). Patients with SIBO & celiac disease showed significantly higher percentages of gammadelta+ IELs (14.6 +/- 8% and 15.7 +/- 13%) compared to IBS patients (4.1 +/- 2.5%, P<0.05). The results of the study indicate that gammadelta+ IELs might play a crucial role against intestinal bacterial infections. Journal of Clinical Gastroenterology. 2007 Aug;41(7):671-676 health writer who lives in San Francisco and is a frequent author of articles for Celiac.com.
  7. J Pediatr Gastroenterol Nutr. 2004 Feb; 38(2): 177-180 Celiac.com 02/13/2004 - It has been determined that children with celiac disease exhibit an increased level of chromosome aberrations in peripheral blood lymphocytes, which may be a major factor in their higher risk of cancer over time. Now, a study by British and Croatian researchers has found that adherence to a gluten-free diet can actually decrease the number of chromosome aberrations in these children. The researchers compared chromosome aberrations in 17 children with celiac disease--before going gluten-free, then after a minimum 24 month gluten-free diet--and compared these results with that of 15 healthy children. They found that 12 of the 15 celiacs strictly followed the gluten-free diet, and these children had a significantly lower number of chromosome aberrations when compared with both the control group and the other three celiac children who did not follow the diet. The researchers conclude: "The frequency of chromosome aberrations in peripheral blood lymphocytes of patients with celiac disease decreased significantly on a gluten-free diet. We conclude that genomic instability is a secondary phenomenon, possibly caused by chronic intestinal inflammation."
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