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Showing results for tags 'cells'.
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Celiac.com 03/31/2020 - There are over one-hundred different autoimmune diseases. One thing they have in common is that they are driven by the body's own cells; by rare and elusive immune cells that target the body's own healthy organs and tissues, instead of harmful foreign bacteria and viruses. Researchers call such cells 'rogue cells." For the first time, a team led by researchers at the Garvan Institute of Medical Research have used patient samples to document the existence of specific cells that cause autoimmune disease. They also figured out the mechanism that allows cells to 'go rogue' by evading checkpoints that normally stop immune cells from targeting the body's own tissues. "We have developed a technique that allows us to look directly at the cells that cause autoimmune disease—it's as though we're looking through a new microscope lens for the first time, learning more about autoimmune disease than was ever possible before," says Professor Chris Goodnow, co-senior author of the paper, and Executive Director of the Garvan Institute and Director of the UNSW Sydney Cellular Genomics Futures Institute. Potential for New Diagnosis and Treatments In addition to revealing the root cause of an autoimmune disease, the research findings offer huge potential for future treatments to target the cause of all autoimmune diseases. "Current treatments for autoimmune disease address only the symptoms, but not the cause. To make more targeted treatments that address disease development and progression, we first need to understand the cause...Identifying these rogue immune cells is a significant step forward for how we study autoimmune disease—and crucially the first step to finding ways to eliminate them from the body entirely," says Professor Goodnow. "In our study, we uncovered specific mutations that mark early stages of autoimmune disease. If we can diagnose a patient at these stages, it may be possible to combine our knowledge of these mutations with new targeted treatments for lymphoma to intervene in disease progression or to track how well a patient is responding to treatments," says Dr. Reed. The researchers are now planning follow-up studies to investigate mutations of autoimmune cells in a range of other diseases, including lupus, celiac disease and type 1 diabetes. The team's findings, published in the journal Cell today, are part of the visionary Hope Research program, could lead to major advances in the diagnosis and treatment of autoimmune disease. Read more in MedicalExpressNews.com -
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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 -
Celiac.com 07/18/2016 - Researchers still don't have a very good understanding about what triggers non-celiac wheat sensitivity. To get a better idea, a team of researchers recently set out to examine the inflammatory response in the rectal mucosa of patients with well-defined non-celiac wheat sensitivity. Specifically, they wanted to look at type 1 innate lymphoid cells in the rectal mucosa of those patients. The research team included Diana Di Liberto, Pasquale Mansueto, Alberto D'Alcamo, Marianna Lo Pizzo, Elena Lo Presti1, Girolamo Geraci, Francesca Fayer, Giuliana Guggino, Giuseppe Iacono, Francesco Dieli, and Antonio Carroccio. They are variously affiliated with the Central Laboratory of Advanced Diagnosis and Biomedical Research (CLADIBIOR), University of Palermo, Palermo, Italy, the Dipartimento di Biopatologia e Biotecnologie Mediche (DIBIMED), University of Palermo, Palermo, Italy, the Dipartimento Biomedico di Medicina Interna e Specialistica (DIBIMIS), University of Palermo, Palermo, Italy, the Surgery Department at the University of Palermo in Palermo, Italy, and with the Pediatric Gastroenterology, ARNAS Di Cristina Hospital, Palermo, Italy 6Internal Medicine, Giovanni Paolo II Hospital, Sciacca (ASP Agrigento), Palermo, Italy. For their study, the team included 22 patients with irritable bowel syndrome (IBS)-like clinical presentation, diagnosed with non-celiac wheat sensitivity by double-blind placebo-controlled challenge. As control subjects, they used eight IBS patients who were not improving on wheat-free diet. Two weeks after each of the subjects consumed 80 grams of wheat daily as part of an oral challenge, the researchers isolated cells from rectal biopsies and thoroughly characterized them using fluorescence-activated cell sorting analysis for intracellular cytokines and surface markers. Analysis of the rectal biopsies of wheat-challenged non-celiac wheat sensitivity patients showed that a significant mucosal CD45+ infiltrate consisted of CD3+ and CD3− lymphocytes, with the latter spontaneously producing more interferon (IFN)-γ than IBS controls. About 30% of IFN-γ-producing CD45+ cells were T-bet+, CD56−, NKP44−, and CD117−, defining them as a type-1 innate lymphoid cells (ILC1). IFN-γ-producing ILC1 cells significantly decreased in 10 patients analyzed 2 weeks after they resumed a wheat-free diet. This study shows that IFN-γ-producing ILC1 cells infiltrate rectal mucosa, promoting the lymphoid cell population, which gives rise to non-celiac wheat sensitivity. Source: Clinical and Translational Gastroenterology, 2016 doi:10.1038/ctg.2016.35
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Effector and Suppressor T cells in Celiac Disease
Jefferson Adams posted an article in Latest Research
Celiac.com 08/17/2015 - In an interesting update, researcher Giuseppe Mazzarella, of the Immuno-Morphology Lab at the Institute of Food Sciences of the National Council Research in Avellino, Italy recently set out to examine the role of effector and suppressor T cells in celiac. Celiac disease is a T-cell-mediated immune disorder in which gliadin-derived peptides activate lamina propria effector CD4+ T cells. This activation triggers the release of cytokines, compatible with a Th1-like pattern, which play a crucial role in the development of celiac disease, and which control many aspects of the inflammatory immune response. Previous studies revealed that a novel subset of effector T cells, marked by expression of high levels of IL-17A, termed Th17 cells, plays a key role in celiac disease. Although these effector T cell subsets produce pro-inflammatory cytokines, which cause significant tissue damage in celiac sufferers, recent studies have suggested the existence of additional CD4(+) T cell subsets with suppressor functions. These subsets include type 1 regulatory T cells and CD25(+)CD4(+) regulatory T cells, expressing the master transcription factor Foxp3, which have important implications for the development and progression of celiac disease. Source: World J Gastroenterol. 2015 Jun 28;21(24):7349-56. doi: 10.3748/wjg.v21.i24.7349. -
Celiac.com 04/28/2014 - Accumulation of dendritic cells (DCs) in duodenal mucosa is associated with celiac disease. Autophagy protein LC3 has recently been implicated in autoantigen formation. However, its role in celiac disease remains unknown. A team of researchers recently set out to examine role of autophagic protein LC3 expressed by activated DCs in celiac disease. The research team included P. Rajaguru, K. Vaiphei, B. Saikia, and R. Kochhar, with the Department of Histopathology, Post Graduate Institute of Medical Education and Research in Chandigarh, India. The team analyzed thirty celiac disease patients at initial presentation and after 6 months of gluten-free diet (GFD). They examined duodenal biopsies for histological changes and CD11c, CD86, and MAP1LC3A expressions by double immunohistochemistry (IHC). They used Masson's trichrome (MT) staining to determine basement membrane (BM) thickness and Oil Red O (ORO) staining for mucosal lipid deposit. They also conducted polymerase chain reaction (PCR) for the HLA-DQ system. For statistical analysis, they used paired and unpaired t test, chi-square test, Fisher's exact test, and McNemar-Bowker test. A P-value They found HLA-DQ2 and HLA-DQ8 alleles in all study subjects. They also observed thicker BM in 63% of subjects, while 73% of subjects showed ORO-positive lipid in surface lining epithelium. Pre-treatment biopsies showed a higher number DCs expressing LC3, which dropped significantly in follow-up biopsies, and also showed significant reduction in BM thickness and ORO. These results show that histological improvement in duodenal biopsies is connected with less activated DCs expressing autophagic protein, which likely play important role in the development of celiac disease and other autoimmune disorders. Source: Indian J Pathol Microbiol. 2013 Oct-Dec;56(4):342-8. doi: 10.4103/0377-4929.125282.
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Celiac.com 12/12/2012 - In duodenal biopsy samples from people with active celiac disease, the transferrin receptor, CD71, is up-regulated, and promotes retro-transport of secretory immunoglobulin A (SIgA)-gliadin complexes. To better understand how interactions between SIgA and CD71 promote transepithelial transport of gliadin peptides, a team of researchers set out to determine if interactions among secretory immunoglobulin A, CD71, and transglutaminase-2 affect permeability of intestinal epithelial cells to gliadin peptides. The research team included C. Lebreton, S. Ménard, J. Abed, I.C. Moura, R. Coppo, C. Dugave, R.C. Monteiro, A. Fricot, M.G. Traore, M. Griffin, C. Cellier, G. Malamut, N. Cerf-Bensussan, and M. Heyman. They are affiliated with the Mixed Research Unit 989 of the National Institute of Health and Medical Research (INSERM UMR989) in Paris, France. For their study, the team evaluated duodenal biopsy specimens from 8 adults and 1 child with active celiac disease. The team used fluorescence-labeled small interfering RNAs against CD71 to transfect Caco-2 and HT29-19A epithelial cell lines. They used flow cytometry, immunoprecipitation, and confocal microscopy to assess interactions among IgA, CD71, and transglutaminase 2 (Tgase2). They then assessed transcytosis of SIgA-CD71 complexes and intestinal permeability to the gliadin 3H-p31-49 peptide in polarized monolayers of Caco-2 cells. To assess physical interplay between SIgA and CD71 or CD71 and Tgase2 at the apical surface of enterocytes in biopsy samples and monolayers of Caco-2 cells, the team used fluorescence resonance energy transfer and in situ proximity ligation assays. They co-precipitated CD71 and Tgase2 with SIgA, bound to the surface of Caco-2 cells. They found that SIgA-CD71 complexes were internalized and localized in early endosomes and recycling compartments, but not in lysosomes. In the presence of celiac IgA or SIgA against p31-49, transport of intact 3H-p31-49 increased significantly across Caco-2 monolayers, while soluble CD71 or Tgase2 inhibitors interfered with transport. Once it binds to apical CD71, SIgA (with or without gliadin peptides) enters a recycling pathway and avoids lysosomal degradation; this process allows apical-basal transcytosis of bound peptides. This mechanism is assisted by Tgase2 and might be involved in the pathogenesis of celiac disease. Source: Gastroenterology. 2012 Sep;143(3):698-707.e1-4. doi: 10.1053/j.gastro.2012.05.051.
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Celiac.com 12/05/2012 - Regulatory T cells (Tregs) are play a pivotal role in helping our bodies tolerate self-antigens and dietary proteins. Interleukin (IL)-15 is a cytokine that is overly present in the intestines of patients with celiac disease. Studies have shown that Interleukin (IL)-15 does not interfere with the generation of functional Tregs, but causes human T cells to resist Treg suppression. To better understand how control of effector T cells by regulatory T cells is inhibited, a team of researchers compared Treg numbers and responses of intestinal and peripheral T lymphocytes to suppression by Tregs in celiac disease patients and in a control group. The research team included N.B. Hmida, M. Ben Ahmed, A. Moussa, M.B. Rejeb, Y. Said, N. Kourda, B. Meresse, M. Abdeladhim, H. Louzir, and N. Cerf-Bensussan. They are affiliated with the Department of Clinical Immunology and the Institut Pasteur de Tunis in Tunis, Tunisia. For their study, the team isolated intraepithelial lymphocytes (IELs) and lamina propria lymphocytes (LPLs) from duodenal biopsy specimens of patients with celiac disease and in a control group. The team then purified CD4+CD25+ T lymphocytes (Tregs) from blood. By analyzing anti-CD3-induced proliferation and interferon (IFN)-γ production in the presence or absence of peripheral Tregs, they were able to test responses of IELs, of LPLs, and peripheral lymphocytes (PBLs) to suppression by Tregs. The team used flow cytometry to measure lamina propria and peripheral CD4+CD25+FOXP3+ T cells. They found that, although patients with active celiac disease showed significantly increased percentages of CD4+CD25+FOXP3+ LPLs, they also showed less inhibited proliferation and IFN-γ production of intestinal T lymphocytes by autologous or heterologous Tregs (P < 0.01). IEL for subjects with celiac disease showed no response to Tregs. Also, the team noted resistance of LPLs and PBLs to Treg suppression in patients with villous atrophy who had substantially higher blood levels of IL-15 compared with patients without villous atrophy and controls. From their results, the research team concludes that effector T lymphocytes in people with active celiac disease become resistant to suppression by Tregs. This resistance may result in loss of tolerance to gluten, and to self-antigens. Source: Am J Gastroenterol. 2012 Apr;107(4):604-11. doi: 10.1038/ajg.2011.397. Epub 2011 Nov 22.
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Celiac.com 09/21/2012 - Refractory celiac disease type II (RCDII) is a severe complication of celiac disease that occurs when symptoms and intestinal damage continue even when the patient adopt a gluten-free diet. Refractory celiac disease marked by abnormal intraepithelial lymphocytes (IELs) of unknown origin that display an atypical CD3(-)CD7(+)icCD3(+) phenotype. About 40% of patients with RCDII lymphocytes develop a dangerous and invasive lymphoma. A team of researchers recently sought to identify possible origins of abnormal intraepithelial lymphocytes in refractory celiac disease type II. The research team included F. Schmitz; T.M. Tjon, Y. Lai; A. Thompson; Y. Kooy-Winkelaar; R.J. Lemmers; H.W. Verspaget; M.L. Mearin; F.J. Staal; M.W. Schreurs; T. Cupedo; A.W. Langerak; C.J. Mulder; J. van Bergen; and F. Koning. In their study, the researches sought to find the physiological counterpart of these abnormal intraepithelial lymphocytes cells. To do so, they used microarray analysis, real-time quantitative PCR and flow cytometry to compare RCDII cell lines with T-cell receptor positive (TCR(+)) IEL (T-IEL) lines. They then used their data to identify cells with an RCDII-associated phenotype in duodenal biopsies from non-refractory individuals by multicolor flow cytometry. They found that RCDII cell lines were distinct from T-IEL lines and showed higher levels of multiple natural killer (NK) cell receptors. In addition to the CD3(-)CD7(+)icCD3(+) phenotype, the RCDII lines showed an absence of CD56, CD127 and CD34, compared with other lymphocyte subsets. Moreover, they found cells matching this surface lineage-negative (Lin(-)) CD7(+)CD127(-)CD34(-) phenotype that showed a functional interleukin-15 (IL-15) receptor and comprised a substantial portion of IELs in duodenal specimens of patients without celiac disease, particularly children. They also found cells of this kind in the thymus. For patients without celiac disease, the Lin(-)CD7(+)CD127(-)CD34(-) subset was one of four subsets within the CD3(-)CD7(+)icCD3(+) population that showed a differential expression of CD56 and/or CD127. The results indicate that the CD3(-)CD7(+)icCD3(+) population is heterogeneous and show the existence of a Lin(-) subset that is different from T, B, NK and lymphoid tissue inducer cells. The team hypothesizes that the IL-15 cells are the counterpart of abnormal cells that are expanded in RCDII and transformed in RCDII-associated lymphoma. Source: Gut. 2012 Jul 6. -
Celiac.com 05/16/2012 - Goblet cells that line the intestine and secrete mucous are emerging as a possible target for treating inflammatory bowel disease, celiac disease and food allergies. With every meal, immune cells in the intestine stand guard against harmful bacteria but permit vitamins and nutrients to pass. The small intestine is protected from harmful pathogens by a layer of mucus secreted from goblet cells. A research team at Washington University School of Medicine in St. Louis have identified the cells that protect the intestine against food antigens, or proteins so that the immune system does not begin an attack. The discovery of goblet cells in mice shines new light on their role in the lining of the intestine, and gives scientists a potential target for treatments against inflammatory bowel disease, celiac disease and food allergies. To accomplish their task, the researchers used a new imaging technique that allows them to observe the inner workings of the intestine in a living mouse in real time. For their study, they fed marked sugar to mice and observed antigens as they were passed by goblet cells to dendritic cells. Dendritic cells play a key role in the immune system. But until now, scientists thought that intestinal goblet cells were only responsible for secreting mucus. Miller and Newberry also studied healthy human intestinal tissue from patients undergoing weight-loss surgery. Those results showed that goblet cells perform the same function in people as in mice. This indicates that the cells may be solid drug targets for treating inflammatory bowel disease and other intestinal problems. After studying normal, healthy mice, the researchers are now using the same imaging technique to look at how goblet cells and dendritic cells might function differently when inflammation or infection occurs. They also plan to study mucus-producing goblet cells in other tissues, such as the lung, to assess whether they are working the same way elsewhere in the body. Miller says the results are important because they help scientists understand that intestinal immune responses may depend as much on the ability of goblet cells to transport antigens to dendritic cells as on what the dendritic cells then do with those antigens. Source: Nature. 2012 Mar 14;483(7389):345-9. doi: 10.1038/nature10863. -
Celiac.com 06/30/2008 - In the crypts of the small bowel, there is a group of small, granular epithelial cells, called Paneth cells, which play an important part in innate immune system. There has been some controversy about what role Paneth cells might play in complicating celiac disease, so team of Italian researchers set out to examine the distribution, proliferation, and function of paneth cells in adults with uncomplicated and complicated celiac disease. The research team was made up of P. Biancheri , Cdel V. Blanco, L. Cantoro, M. De Vincenzi, A. Di Sabatino, W. Dhaliwal, E. Miceli, R. Salerno, A. Vanoli, T.T. Macdonald, and G.R. Corazza. The team is affiliated with the Celiac Specialty Center at the First Department of Medicine at University of Pavia in Pavia, Italy. Seeking to better understand the function and the numbers of Paneth cell adults with celiac disease (celiac disease), the team measured Paneth cells and human alpha-defensin (HD)-5 and HD-6 in 28 adults with uncomplicated celiac disease, 8 patients with complicated celiac disease (3 with ulcerative jejunoileitis, 2 with refractory sprue, and 3 with enteropathy-associated T-cell lymphoma), and 14 control subjects. Subjects with uncomplicated untreated and treated celiac disease showed similar numbers of Paneth cells, with similar cell proliferation, compared to the control group, while subjects with complicated celiac disease showed much fewer Paneth. Subjects with uncomplicated untreated celiac disease, and those with treated celiac disease showed similar levels of mucosal HD-5 and HD-6 compared to the control group, while cells taken from the biopsies of subjects with treated celiac disease and challenged with gliadin proteins showed no change in mucosal HD-5 and HD-6 transcripts. Furthermore, those subjects with uncomplicated celiac disease showed no reduction in mucosal Paneth cell numbers and alpha-defensins. Clearly, a small study such as this will not tell us exactly how a reduction in the numbers of Paneth cells might complicate celiac disease, but since the role of Paneth cells is so vital to healthy innate immune function, it does point to the need for further examination. Am J Clin Pathol. 2008 Jul;130(1):34-42.
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Celiac.com 06/06/2011 - The interplay among the different immune cells mediating intestinal inflammation in celiac disease is complicated indeed. A subset of T regulatory (Treg) cells that express the Foxp3 protein are present in higher numbers in the intestines of patients with active celiac disease than in healthy controls. Treg cells act to suppress the immune system, providing tolerance to self-antigens. A recent report in the American Journal of Gastroenterology demonstrates that these cells proliferate upon the ingestion of gluten in order to suppress an overactive inflammatory response, but that their suppression is in turn suppressed by interleukin-15. First they confirmed that there is in fact increased expression of Foxp3+ cells in the intestinal mucosa of untreated celiac patients; happily, they write that "no significant differences were noted in the number of Foxp3+ cells in biopsy samples of treated celiac disease in comparison with biopsy samples of non-celiac disease controls." Next, they used an in vitro gliadin challenge system - no celiac patients were harmed during the course of this study! - to see if the increase in this cell population was dependent on gliadin, and it was. T cells are so named because they are made in the thymus; this demonstration that they can originate in the small intestine lamina propria is interesting. Treg cells are generally immunosuppressive, and the Treg cells isolated from celiac guts demonstrated this immunosuppressive ability in vitro. So the researchers wondered: why is there still so much inflammation in untreated celiac disease patients? They found that the cytokine IL-15 could suppress the proliferation of Treg cells, and completely shut down their ability to produce interferon gamma (IFN- γ ). This is at least partially because Treg cells from celiac patients turn out to have a significantly higher surface density of receptors for IL-15 than Treg cells from healthy controls, rendering them more sensitive to IL-15's effects. Zanzi et al bolstered their findings by achieving the same results using two independent experimental methods. It is not yet clear how IL-15 impairs the suppressive activity of Treg cells. But these scientists are actively working on it. Source: Am J Gastroenterol advance online publication, 5 April 2011; doi: 10.1038/ajg.2011.80 -
Celiac.com 02/03/2010 - Celiac disease increases production of IL-17A by cells that also make IFN-gamma. Recently, a research team set out to characterize the expression of IL-17A-producing cells in celiac disease. The team included I. Monteleone, M. Sarra, G. Del Vecchio Blanco, O. A. Paoluzi, E. Franzè, D. Fina, A. Fabrizi, T. T. Macdonald, F. Pallone, and G. Monteleone of the Department of Internal Medicine at the University of Tor Vergata in Rome, Italy. Infiltration of the mucosa with IFN-gamma-secreting Th1 cells is one of the features associated with celiac disease. Recent studies have shown the pathogenic effects previously attributed to Th1 cells may in fact be caused by a novel subset of T cells, termed Th17 cells, and noted for expressing high levels of IL-17A. In this study, the team set out to characterize the expression of IL-17A-producing cells in celiac disease. Using real-time PCR and ELISA, the team showed that expression of IL-17A RNA and protein is greater in active celiac disease biopsy specimens than in specimens from inactive celiac disease, and normal mucosal biopsies. Through flow cytometry, the team confirmed that the mucosa of celiac disease patients overproduces IL-17A, and that the main sources for this overproduction were CD4(+) and CD4(+)CD8(+) cells. Most IL-17A-producing CD4(+) and CD4(+)CD8(+) cells co-expressed IFN-gamma but did not co-express CD161. Including a peptic-tryptic digest of gliadin to ex-vivo organ cultures of duodenal biopsy specimens taken from patients with inactive celiac disease enhanced IL-17A production by both CD4(+) and CD4(+)CD8(+) cells. Since the team showed earlier that patients with celiac disease overproduced IL-21, a T cell-derived cytokine involved in the control of Th17 cell responses, they next determined whether IL-21 was responsible for regulating IL-17A expression. Blocking IL-21 action with a neutralizing IL-21 Ab lowered total IL-17A expression in cultures of active celiac disease and peptic-tryptic digest of gliadin-treated celiac disease biopsy specimens. From the data, the team concludes that celiac disease increases IL-17A, which is produced by cells that also produce IFN-gamma. Source: Journal of Immunology, 2010 Jan 8.
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A team of researchers with the Department of Medicine at the University Erlangen-Nuernberg in Germany recently set out to examine the role of the innate immune system in celiac disease. The team included Maryam Rakhimova, Birgit Esslinger, Anja Schulze-Krebs, Eckhart G. Hahn, Detlef Schuppan and Walburga Dieterich. The researchers matured dendritic cells taken from venous blood of patients with both active and with treated celiac disease, along with DQ2–DQ8-positive or negative control subjects. They treated the dendritic cells with a peptic–tryptic digest of gliadin (500 μg/ml) and assessed activation by means of fluorescent-activated cell sorting analysis, cytokine secretion, and the cells' ability to trigger T cell proliferation. The team noted that gliadin up-regulated interleukin (IL)-6, IL-8, and IL-12 (p40) secretion in dendritic cells and triggered clear expression of the maturation markers human leukocyte antigen (HLA)-DR, CD25, CD83, and CD86 in all test subjects, without regard to their genotype or the presence of disease; whereas the digest of bovine serum albumin had no effect. However, gliadin-stimulated dendritic cells from patients with active celiac disease showed greater stimulation of autologous T cells compared to the other groups. The team concluded that further research should be aimed at identifying the mechanisms that control inflammation in healthy individuals. Source: J Clin Immunol, Volume 29, Number 1, January, 2009
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Nature Immunology 2, 353 - 360 (April 2001) Celiac.com 04/12/2001 - According to an article published in the April issue of Nature Immunology, Dr. Marc Rothenberg and colleagues at the Childrens Hospital Medical Center in Cincinnati, Ohio performed a series of experiments on mice which led them to the conclusion that white blood cells called eosinophils could be the cause of many food allergies and gastrointestinal inflammation. The researchers believe that the eosinophil cells, which are present throughout the body, mistakenly identify food proteins as germs in individuals with food allergies. When the intestinal lining of an allergic person is exposed to an allergen, a substance called eotaxin is released by the cells lining the intestine, which causes the eosinophil cells and other immune cells to attack them and release powerful proteins that destroy the surrounding tissues and cause eosinophilic inflammation. The results of this study are unique because this is the first time eosinophils cells have been implicated in causing allergies, even though scientists have known for some time that they were present in great numbers at the sites of inflammation caused by reactions to food. The implication of this study is the possible development of drugs that stop this reaction from occurring, and thus prevent digestive inflammation and destruction that occurs when people with food allergies eat foods to which they are allergic. These results put scientists one step further in understanding how and why the digestive system is attacked in certain individuals, and a possible means of one day controlling the process. -
Celiac.com 03/04/2004 - Kimball Genetics is pleased to announce availability of the One-Day Celiac Disease DNA Test for cheek cell specimens in addition to blood. Cheek cell specimens are popular with both patients and physicians because they eliminate the need for a blood draw and are convenient to collect and ship. Kimball Genetics unique ability to perform celiac disease testing on cheek cells enables direct-to-consumer marketing of this service. Celiac disease is a chronic, autoimmune, gastrointestinal disorder. In genetically susceptible individuals, ingestion of gluten-containing grains, especially wheat, causes inflammation of the small intestine mucosa and leads to malabsorption. Long believed to be a rare disorder, celiac disease is now known to be one of the most common, under-diagnosed diseases, affecting 1:120-1:300 individuals in European and North American populations. Early detection through antibody and genetic testing and subsequent elimination of gluten from the diet is essential in aiding prevention and treatment. Due to the extremely variable presentation of disease symptoms and severity, diagnosing celiac disease is difficult. Antiendomysial and tissue transglutaminase antibody test results can be equivocal depending upon diet adherence and stage of disease. Kimball Genetics One-Day Celiac Disease DNA Test is a reliable and critical tool for accurately diagnosing celiac disease. Kimball Genetics One-Day Celiac Disease DNA Test includes highest accuracy of testing, one-day turnaround time, detailed test reports, free genetic counseling for physicians and patients, and excellent personal service For more information about the Celiac Disease DNA Test, please contact Juli Murphy, M.S. at (800) 320-1807 or at jamurphy@kimballgenetics.com. About Kimball Genetics, Inc. Kimball Genetics, Inc., is an independent genetic testing laboratory with a national reputation for combining the highest accuracy of testing with unparalleled turnaround time and excellent personal service. Founded in 1994 by Annette K. Taylor, M.S., Ph.D., Kimball Genetics has distinguished itself from other molecular diagnostic labs by its one-day turnaround time and unique emphasis on genetic counseling and education. For: Kimball Genetics, Inc., 101 University Blvd., Suite 350, Denver, CO 80206 Contact: Juli Murphy, M.S., (800) 320-1807
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