Influence of CD26/dipeptidyl peptidase IV deficiency on immunophenotypic changes during colitis development and resolution

Detel, Dijana; Buljević, Sunčica; Batičić, Lara; Kučić, Natalia; Pugel, Ester Pernjak; Varljen, Jadranka

doi:10.1007/s13105-016-0491-7

Cited by 15 publications

(13 citation statements)

References 38 publications

(49 reference statements)

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“…To investigate the influence of DPP-4 in the pathogenesis of DSS-induced colitis, DPP-4-deficient mice were used in DSS treatment, and an increase of myeloperoxidase (MPO) activity and expression of NF-κB p65 subunit in the colonic tissues was observed. Furthermore, an increase in the percentage of splenic CD8 + cells and NKT cells in CD26-deficient mice was observed ( 100 ). In keeping with GLP-2-treated mice, DPP-4-deficient mice also showed a significant increase in macrophages when compared with wild-type mice ( 101 ).…”

Section: Inhibition Of Dpp-4 Function In Ibdmentioning

confidence: 99%

Role of Incretin Axis in Inflammatory Bowel Disease

et al. 2017

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The inflammatory bowel diseases (IBDs), including Crohn’s disease (CD) and ulcerative colitis (UC), are chronic inflammatory conditions of the gastrointestinal tract and involve a complicated reciprocity of environmental, genetic, and immunologic factors. Despite substantial advances in the foundational understanding of the immunological pathogenesis of IBD, the detailed mechanism of the pathological progression in IBD remains unknown. In addition to Th1/Th2 cells, whose role in IBD has been previously well defined, recent evidence indicates that Th17 cells and Tregs also play a crucial role in the development of IBD. Diets which contain excess sugars, salt, and fat may also be important actors in the pathogenesis of IBD, which may be the cause of high IBD incidence in western developed and industrialized countries. Up until now, the reason for the variance in prevalence of IBD between developed and developing countries has been unknown. This is partly due to the increasing popularity of western diets in developing countries, which makes the data harder to interpret. The enterocrinins glucagon-like peptides (GLPs), including GLP-1 and GLP-2, exhibit notable benefits on lipid metabolism, atherosclerosis formation, plasma glucose levels, and maintenance of gastric mucosa integrity. In addition to the regulation of nutrient metabolism, the emerging role of GLPs and their degrading enzyme dipeptidyl peptidase-4 (DPP-4) in gastrointestinal diseases has gained increasing attention. Therefore, here we review the function of the DPP-4/GLP axis in IBD.

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Section: Inhibition Of Dpp-4 Function In Ibdmentioning

confidence: 99%

Role of Incretin Axis in Inflammatory Bowel Disease

et al. 2017

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“…In DPP-IVdeficient mice induction of colitis by DSS resulted in a stronger increase of myeloperoxidase activity and expression of NF-B p65 subunit in the colonic tissue compared with wildtype mice (Detel et al 2016). Furthermore, in DPP-IV deficient mice, increase in the percentage of splenic CD+ cells and NKT cells as well as increase in macrophages was observed (Detel et al 2016). Salaga et al (2017) demonstrated that EMDB-1, a new peptide analog of endomorphin-2, with a potential to inhibit DPP-IV ameliorated colonic inflammation in both DSS-and TNBS-induced mouse model of colitis.…”

Section: Inhibition Of Dpp-iv As a Potential Therapeutic Strategy In Ibdmentioning

confidence: 94%

“…It has been proposed that the protective effect of DPP-IV inhibition may be a result of increased levels of GLP-1 and GLP-2 (Yazbeck et al 2010b;Ban et al 2011). Detel et al investigated the role of DPP-IV in the pathogenesis of colitis (Detel et al 2016). In DPP-IVdeficient mice induction of colitis by DSS resulted in a stronger increase of myeloperoxidase activity and expression of NF-B p65 subunit in the colonic tissue compared with wildtype mice (Detel et al 2016).…”

Section: Inhibition Of Dpp-iv As a Potential Therapeutic Strategy In Ibdmentioning

confidence: 99%

“…Detel et al investigated the role of DPP-IV in the pathogenesis of colitis (Detel et al 2016). In DPP-IVdeficient mice induction of colitis by DSS resulted in a stronger increase of myeloperoxidase activity and expression of NF-B p65 subunit in the colonic tissue compared with wildtype mice (Detel et al 2016). Furthermore, in DPP-IV deficient mice, increase in the percentage of splenic CD+ cells and NKT cells as well as increase in macrophages was observed (Detel et al 2016).…”

Section: Inhibition Of Dpp-iv As a Potential Therapeutic Strategy In Ibdmentioning

confidence: 99%

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Role of glucagon-like peptides in inflammatory bowel diseases—current knowledge and future perspectives

Zatorski

Sałaga

Fichna

2019

Naunyn-Schmiedeberg's Arch Pharmacol

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Inflammatory bowel diseases (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), are chronic, relapsing, intestinal inflammatory disorders with complex and yet unrevealed pathogenesis in which genetic, immunological, and environmental factors play a role. Nowadays, a higher proportion of elderly IBD patients with coexisting conditions, such as cardiovascular disease and/or diabetes is recorded, who require more complex treatment and became a great challenge for gastroenterologists. Furthermore, some patients do not respond to anti-IBD therapy. These facts, together with increasing comorbidities in patients with IBD, imply that urgent, more complex, novel therapeutic strategies in the treatment are needed. Glucagon-like peptides (GLPs) possess numerous functions in the human body such as lowering blood glucose level, controlling body weight, inhibiting gastric emptying, reducing food ingestion, increasing crypt cell proliferation, and improving intestinal growth and nutrient absorption. Thus, GLPs and dipeptidyl peptidase IV (DPP-IV) inhibitors have recently gained attention in IBD research. Several animal models showed that treatment with GLPs may lead to improvement of colitis. This review presents data on the multitude effects of GLPs in the inflammatory intestinal diseases and summarizes the current knowledge on GLPs, which have the potential to become a novel therapeutic option in IBD therapy.

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“…CD26 is expressed at high level by several T cell subsets including Th17 cells [15] and mucosal-associated invariant T cells (MAIT cells) [16]. Gene knockout mouse studies indicate that CD26 plays both T cell activating [17] and modulatory functions [18].…”

Section: Ucb Derived Foxp3+ T Cells Uniquely Express Cd26 and Cd31mentioning

confidence: 99%

CD36^himonocytes play immunoregulatory roles in human umbilical cord blood

Seki

et al. 2018

Preprint

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The fetal and neonatal immune systems are uniquely poised to generate tolerance to self, maternal, and environmental antigens encountered in the womb and shortly after birth. The tolerogenic nature of fetal and neonatal immunity is a rising health concern with the spread of vertically transmitted viruses, such as the Zika virus. A variety of mechanisms contribute to fetal and neonatal tolerance, including a propensity to generate Foxp3+ regulatory T cells (Tregs). Here, we demonstrate that a subset of CD14+ monocytes expressing the scavenger molecule, CD36, is able to generate CD4+ and CD8+ T cells that express Foxp3 from umbilical cord blood (UCB). Monocyte-induced Foxp3+ T cells have potent suppressive functions on T cell proliferation and maintain Foxp3 expression over six weeks in vitro. Importantly, UCB-derived Foxp3+ T cells are distinguishable from adult peripheral blood (APB) CD4+CD25+ Tregs by surface antigen expression. While UCB-derived Foxp3+ T cells express prototypic Treg-associated surface antigens, such as CD25 and glucocorticoid-induced tumor necrosis factor-related receptor (GITR), only UCB-derived Foxp3+ T cells express CD26. In addition, most UCB-derived CD8+Foxp3+ T cells express CD31. Mechanistically, both APB and UCB-derived monocytes support the development of Foxp3+ T cells from naïve T cells, but APB naïve T cells are less efficient in expressing Foxp3 than UCB naïve T cells. These data suggest that antigen presentation by CD36hi monocytes in the fetus leads to the development of a group of T cells that share some but not all phenotypes of adult thymus-derived Tregs.

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Influence of CD26/dipeptidyl peptidase IV deficiency on immunophenotypic changes during colitis development and resolution

Cited by 15 publications

References 38 publications

Role of Incretin Axis in Inflammatory Bowel Disease

Role of Incretin Axis in Inflammatory Bowel Disease

Role of glucagon-like peptides in inflammatory bowel diseases—current knowledge and future perspectives

CD36^himonocytes play immunoregulatory roles in human umbilical cord blood

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Influence of CD26/dipeptidyl peptidase IV deficiency on immunophenotypic changes during colitis development and resolution

Cited by 15 publications

References 38 publications

Role of Incretin Axis in Inflammatory Bowel Disease

Role of Incretin Axis in Inflammatory Bowel Disease

Role of glucagon-like peptides in inflammatory bowel diseases—current knowledge and future perspectives

CD36himonocytes play immunoregulatory roles in human umbilical cord blood

Contact Info

Product

Resources

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CD36^himonocytes play immunoregulatory roles in human umbilical cord blood