scholarly journals The role of UVR and vitamin D on T cells and inflammatory bowel disease

2017 ◽  
Vol 16 (3) ◽  
pp. 347-353 ◽  
Author(s):  
Stephanie Bora ◽  
Margherita T. Cantorna
Keyword(s):  
Inflammatory Bowel Disease ◽  
Vitamin D ◽  
T Cells ◽  
Bowel Disease ◽  
Inflammatory Bowel

Vitamin D/UVR effects on T cells that are important in the development of inflammatory bowel disease (IBD).

scholarly journals TRAIL suppresses gut inflammation and inhibits colitogeic T-cell activation in experimental colitis via an apoptosis-independent pathway

2019 ◽  
Vol 12 (4) ◽  
pp. 980-989 ◽  
Author(s):  
I. T. Chyuan ◽  
H. F. Tsai ◽  
C. S. Wu ◽  
P. N. Hsu
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cells ◽  
T Cell ◽  
T Cell Activation ◽  
Bowel Disease ◽  
Cell Activation ◽  
Gut Inflammation ◽  
Inflammatory Bowel ◽  
Colitis Model

AbstractTumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces cell apoptosis by transducing apoptosis signals. Recently, accumulating evidence demonstrated that TRAIL regulates autoimmune inflammation and immune cell homeostasis in several autoimmune animal models, suggesting a novel immunoregulatory role of TRAIL in autoimmune diseases. However, the impact of TRAIL in inflammatory bowel disease is yet undefined. This study is to address the therapeutic effects and immunoregulatory role of TRAIL in autoimmune gut inflammation. We demonstrated herein that TRAIL significantly suppressed gut inflammation and reduced the severity of colitis in a dextran sodium sulfate (DSS)-induced colitis model. Suppression of gut inflammation was not due to induction of apoptosis in colonic T cells, dendritic cells, or epithelium cells by TRAIL. In contrast, TRAIL directly inhibited activation of colitogenic T cells and development of gut inflammation in an adoptive transfer-induced colitis model. The anti-inflammatory effects of TRAIL on colitis were abolished when T cells from TRAIL receptor (TRAIL-R) knockout mice were adoptively transferred, suggesting that TRAIL regulates autoreactive colitogenic T-cell activation in the development of gut inflammation. Our results demonstrate that TRAIL effectively inhibited colonic T-cell activation and suppressed autoimmune colitis, suggesting a potential therapeutic application of TRAIL in human inflammatory bowel disease.

scholarly journals New Insights on CD8+ T Cells in Inflammatory Bowel Disease and Therapeutic Approaches

2021 ◽  
Vol 12 ◽  
Author(s):  
Rosaely Casalegno Garduño ◽  
Jan Däbritz
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cells ◽  
Cd8 T Cells ◽  
Bowel Disease ◽  
Positive Outcome ◽  
T Cell Subsets ◽  
Therapeutic Approaches ◽  
Therapeutic Value ◽  
Inflammatory Bowel

CD8+ T cells are involved in the pathogenesis of inflammatory bowel disease (IBD), a complex multifactorial chronic disease. Here, we present an overview of the current research with the controversial findings of CD8+ T cell subsets and discuss some possible perspectives on their therapeutic value in IBD. Studies on the role of CD8+ T cells in IBD have contradictory outcomes, which might be related to the heterogeneity of the cells. Recent data suggest that cytotoxic CD8+ T cells (Tc1) and interleukin (IL) 17-producing CD8+ (Tc17) cells contribute to the pathogenesis of IBD. Moreover, subsets of regulatory CD8+ T cells are abundant at sites of inflammation and can exhibit pro-inflammatory features. Some subsets of tissue resident memory CD8+ T cells (Trm) might be immunosuppressant, whereas others might be pro-inflammatory. Lastly, exhausted T cells might indicate a positive outcome for patients. The function and plasticity of different subsets of CD8+ T cells in health and IBD remain to be further investigated in a challenging field due to the limited availability of mucosal samples and adequate controls.

scholarly journals The Role of Vitamin D in the Pathogenesis of Inflammatory Bowel Disease

2019 ◽  
Vol 1 (1) ◽  
pp. 231-240 ◽  
Author(s):  
Stefano Nobile ◽  
Michela Tenace ◽  
Helen Pappa
Keyword(s):  
Inflammatory Bowel Disease ◽  
Vitamin D ◽  
Immune System ◽  
Bowel Disease ◽  
Immune Dysregulation ◽  
Proof Of Concept ◽  
Search Terms ◽  
System Components ◽  
Inflammatory Bowel

Vitamin D has a complex role in the pathogenesis of inflammatory bowel disease (IBD), which is still under investigation. We conducted a literature search using PubMed through December 2018 through the use of relevant search terms. We found an abundance of evidence to support the role of vitamin D in regulating the innate and adaptive arms of the immune system. The pathogenesis of IBD implicates the immune dysregulation of these immune system components. Proof of concept of the vitamin’s role in the pathogenesis of IBD is the mapping of the vitamin D receptor in a region of chromosome 12, where IBD is also mapped, and specific VDR polymorphisms’ link to IBD phenotypes. Further research is needed to better delineate vitamin D’s role in preventing IBD and its potential as a therapeutic target for this disease.

Role of miR-22 in intestinal mucosa tissues and peripheral blood CD4+ T cells of inflammatory bowel disease

2018 ◽  
Vol 214 (8) ◽  
pp. 1095-1104 ◽  
Author(s):  
Xu-Feng Pei ◽  
Long-Lei Cao ◽  
Fang Huang ◽  
Xu Qiao ◽  
Jie Yu ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cells ◽  
Intestinal Mucosa ◽  
Bowel Disease ◽  
Peripheral Blood ◽  
Cd4 T Cells ◽  
Inflammatory Bowel

scholarly journals CCR4-dependent regulatory T cell function in inflammatory bowel disease

2007 ◽  
Vol 204 (6) ◽  
pp. 1327-1334 ◽  
Author(s):  
Qian Yuan ◽  
Shannon K. Bromley ◽  
Terry K. Means ◽  
Krister J. Jones ◽  
Fumitaka Hayashi ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cells ◽  
Adoptive Transfer ◽  
Bowel Disease ◽  
Transfer Model ◽  
Time Points ◽  
Suppressive Function ◽  
Inflammatory Bowel

Inflammatory bowel disease (IBD) is an idiopathic inflammatory disease of the intestine. CD4+ T lymphocytes play an important role in both initiating and regulating intestinal inflammatory immune responses. CD4+CD25+CD45RBlow regulatory T (T reg) cells are capable of preventing the development of colitis in a mouse model of IBD. The precise mechanism of T reg cell–mediated prevention of colitis in this model is unclear, and the role of chemokine receptors in the trafficking and function of T reg cells in this model has not been determined. We examined the role of the chemokine receptor CCR4 in in vivo trafficking and suppressive function of T reg cells in a mouse adoptive transfer model of IBD. CCR4-deficient T reg cells failed to accumulate in the mesenteric lymph nodes (MLNs) at early time points (2–5 d) after adoptive transfer, resulting in a failure to suppress the generation of pathogenic T cells and the development of colitis. Moreover, although CCR4-deficent T cells had equivalent in vitro suppressive activity and accumulated in MLNs at later time points (42–56 d), they were unable to suppress colitis. Our study demonstrates that CCR4 plays an important role in T reg cell trafficking in LNs and that this is critical for T reg cell suppressive function in vivo.

Helicobacter-induced inflammatory bowel disease in IL-10- and T cell-deficient mice

2001 ◽  
Vol 281 (3) ◽  
pp. G764-G778 ◽  
Author(s):  
Andrew Burich ◽  
Robert Hershberg ◽  
Kim Waggie ◽  
Weiping Zeng ◽  
Thea Brabb ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cells ◽  
T Cell ◽  
T Lymphocytes ◽  
Bowel Disease ◽  
Wild Type ◽  
Immunodeficient Mice ◽  
Inflammatory Bowel ◽  
Rag 1

Inflammatory bowel disease (IBD) is thought to result from a dysregulated mucosal immune response to luminal microbial antigens, with T lymphocytes mediating the colonic pathology. Infection with Helicobacter spp has been reported to cause IBD in immunodeficient mice, some of which lack T lymphocytes. To further understand the role of T cells and microbial antigens in triggering IBD, we infected interleukin (IL)-10−/−, recombinase-activating gene (Rag)1−/−, T-cell receptor (TCR)-α−/−, TCR-β−/−, and wild-type mice with Helicobacter hepaticus or Helicobacter bilis and compared the histopathological IBD phenotype. IL-10−/−mice developed severe diffuse IBD with either H. bilis or H. hepaticus, whereas Rag1−/−, TCR-α−/−, TCR-β−/−, and wild-type mice showed different susceptibilities to Helicobacter spp infection. Proinflammatory cytokine mRNA expression was increased in the colons of Helicobacter-infected IL-10−/−and TCR-α−/−mice with IBD. These results confirm and extend the role of Helicobacter as a useful tool for investigating microbial-induced IBD and show the importance, but not strict dependence, of T cells in the development of bacterial-induced IBD.

scholarly journals Vitamin D and Inflammatory Bowel Disease

2015 ◽  
Vol 2015 ◽  
pp. 1-16 ◽  
Author(s):  
Marco Ardesia ◽  
Guido Ferlazzo ◽  
Walter Fries
Keyword(s):  
Inflammatory Bowel Disease ◽  
Vitamin D ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Vitamin D Receptor ◽  
Bowel Disease ◽  
Vitamin D Levels ◽  
Inflammatory Bowel ◽  
Low Serum

Vitamin D deficiency has been recognized as an environmental risk factor for Crohn’s disease since the early 80s. Initially, this finding was correlated with metabolic bone disease. Low serum 25-hydroxyvitamin D levels have been repeatedly reported in inflammatory bowel diseases together with a relationship between vitamin D status and disease activity. Subsequently, low serum vitamin D levels have been reported in various immune-related diseases pointing to an immunoregulatory role. Indeed, vitamin D and its receptor (VDR) are known to interact with different players of the immune homeostasis by controlling cell proliferation, antigen receptor signalling, and intestinal barrier function. Moreover, 1,25-dihydroxyvitamin D is implicated in NOD2-mediated expression of defensin-β2, the latter known to play a crucial role in the pathogenesis of Crohn’s disease (IBD1 gene), and several genetic variants of the vitamin D receptor have been identified as Crohn’s disease candidate susceptibility genes. From animal models we have learned that deletion of the VDR gene was associated with a more severe disease. There is a growing body of evidence concerning the therapeutic role of vitamin D/synthetic vitamin D receptor agonists in clinical and experimental models of inflammatory bowel disease far beyond the role of calcium homeostasis and bone metabolism.

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