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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 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.