scholarly journals The Immunopathology of Sepsis: Pathogen Recognition, Systemic Inflammation, the Compensatory Anti-Inflammatory Response, and Regulatory T Cells

2012 ◽  
Vol 26 (3) ◽  
pp. 457-482 ◽  
Author(s):  
D.H. Lewis ◽  
D.L. Chan ◽  
D. Pinheiro ◽  
E. Armitage-Chan ◽  
O.A. Garden
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Inflammatory Response ◽  
Systemic Inflammation ◽  
Pathogen Recognition ◽  
Anti Inflammatory

scholarly journals Atorvastatin Improves Inflammatory Response in Atherosclerosis by Upregulating the Expression of GARP

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Xiaoqi Zhao ◽  
Yuzhou Liu ◽  
Yucheng Zhong ◽  
Bo Liu ◽  
Kunwu Yu ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Inflammatory Response ◽  
Cd4 T Cells ◽  
Biological Membrane ◽  
Atherosclerotic Plaques ◽  
Anti Inflammatory ◽  
The Stability ◽  
Membrane Molecule ◽  
Progression Of Atherosclerosis

Regulatory T cells play an important role in the progression of atherosclerosis. GARP is a newly biological membrane molecule existed on activated Tregs, which is related to the release of TGF-β. The antiatherosclerosis effects of statins partly depend on their multiple immune modulatory potencies. In this paper, we present that atorvastatin could upregulate the expression of GARP and TGF-βin CD4+ T cells and increase the numbers of CD4+LAP+ and CD4+Foxp3+ regulatory T cells in ApoE−/− mice. Also, we indicate that atorvastatin promotes the aggregation of GARP+ and Foxp3+ cells and secretory of the TGF-β1 in atherosclerotic plaques. Furthermore, we prove that atorvastatin could delay the procession of atherosclerosis and improve the stability of atherosclerotic plaques. Interestingly, we report that inhibition of GARP distinctly inhibits the anti-inflammatory effects of atorvastatin. We conclude that atorvastatin improves the inflammatory response in atherosclerosis partly by upregulating the expression of GARP on regulatory T cells.

The novel role of IL-37 to enhance the anti-inflammatory response of regulatory T cells in patients with peripheral atherosclerosis

Vascular ◽  
2020 ◽  
Vol 28 (5) ◽  
pp. 629-642 ◽  
Author(s):  
Hassan Lotfy ◽  
Marwa Moaaz ◽  
Mai Moaaz
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Inflammatory Response ◽  
Transforming Growth Factor Beta ◽  
Lower Limb ◽  
Transforming Growth Factor ◽  
Severe Disease ◽  
Cytokine Secretion ◽  
Enzyme Linked Immunosorbent Assay ◽  
Anti Inflammatory

Objectives Regulatory T cells (Tregs) mediate immunomodulation and protect against atherosclerosis. It is considered that reducing the amount of pro-inflammatory mediators could be achieved by enhancing the anti-inflammatory response, and this may be considered one of the main targets for therapy development. The inhibitory cytokines secreted by Tregs mainly include interleukin-10 (IL-10) and transforming growth factor-beta (TGF-β). Based on its known immunosuppressive involvement with other inflammatory disorders, we hypothesized that the newly characterized cytokine interleukin-37 (IL-37) might be associated with the inhibitory functions of Treg in atherosclerosis. Immune regulatory functions of IL-37 have not been completely clarified. Accordingly, we speculated that IL-37 might play a regulatory role in the immunosuppression of Tregs in atherosclerotic disease. Methods Real-time polymerase chain reaction and enzyme linked immunosorbent assay were used to test gene expression and protein levels of IL-37 in peripheral blood and localized freshly resected arterial tissues from 84 patients with peripheral arterial occlusive disease and 50 non-atherosclerotic subjects. Results were correlated to disease hallmarks. We also evaluated the ability of recombinant IL-37 to modulate Treg cytokine secretion and T cell inhibition in relation to atherosclerotic disorder in vitro. Results: Our results revealed that IL-37 was increased in patients with chronic lower limb atherosclerotic ischemia, compared to non-atherosclerotic controls. In addition, the expression levels of circulating IL-37 correlated with disease severity of chronic lower limb ischemia. Supplementation with rIL-37 augmented levels of released IL-10 and TGF-β in supernatants of T cells co-cultured with Tregs in the enrolled patients. Conclusions: Results suggest a role for IL-37 in mediating anti-inflammatory functions in the atherosclerotic process, potentially involving enhancement of Treg inhibitory function and anti-inflammatory cytokine secretion with a particularly marked direct response in severe disease.

scholarly journals CD4+CD25+Foxp3+ regulatory T cells regulate immune balance in unexplained recurrent spontaneous abortion via the Toll-like receptor 4/nuclear factor-κB pathway

2020 ◽  
Vol 48 (12) ◽  
pp. 030006052098094
Author(s):  
Shuang Qin ◽  
Li Li ◽  
Jia Liu ◽  
Jinrui Zhang ◽  
Qing Xiao ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Inflammatory Response ◽  
Mouse Model ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Unexplained Recurrent Spontaneous Abortion ◽  
Tlr4 Antagonist

Objective The present study aimed to evaluate the effects of cluster of differentiation (CD)4+CD25+ forkhead box p3 (Foxp3)+ regulatory T cells (Tregs) on unexplained recurrent spontaneous abortion (URSA) and the associated mechanisms. Methods The proportion of CD4+CD25+Foxp3+ Tregs and inflammatory cytokine concentrations in the peripheral blood of women with URSA were measured by flow cytometry and enzyme-linked immunosorbent assay, respectively. CBA/JxDBA/2J mating was used to establish an abortion-prone mouse model and the model mice were treated with the Toll-like receptor 4 (TLR4) antagonist E5564 and the TLR4 agonist lipopolysaccharide. Results The proportion of CD4+CD25+Foxp3+ Tregs was decreased and the inflammatory response was increased in women with URSA. In the abortion-prone mouse model, E5564 significantly increased the proportion of CD4+CD25+Foxp3+ Tregs, decreased the inflammatory response, and increased Foxp3 mRNA and protein expression. Lipopolysaccharide had adverse effects on the abortion-prone model. Conclusions These data suggest that CD4+CD25+Foxp3+ Tregs regulate immune homeostasis in URSA via the TLR4/nuclear factor-κB pathway, and that the TLR4 antagonist E5564 may be a novel and potential drug for treating URSA.

Anti-inflammatory effects ofArtemisia princepsin antigen-stimulated T cells and regulatory T cells

2009 ◽  
Vol 61 (8) ◽  
pp. 1043-1050 ◽  
Author(s):  
Sung HoChang ◽  
Eun Jung Jung ◽  
Youn Hee Park ◽  
Dong Gyun Lim ◽  
Na Young Ko ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Anti Inflammatory

scholarly journals The TLR9 Agonist Cobitolimod Induces IL10-Producing Wound Healing Macrophages and Regulatory T Cells in Ulcerative Colitis

2019 ◽  
Vol 14 (4) ◽  
pp. 508-524 ◽  
Author(s):  
Heike Schmitt ◽  
Julia Ulmschneider ◽  
Ulrike Billmeier ◽  
Michael Vieth ◽  
Patrizio Scarozza ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Wound Healing ◽  
T Cells ◽  
Regulatory T Cells ◽  
Th17 Cells ◽  
Experimental Colitis ◽  
Foxp3 Expression ◽  
Treg Cells ◽  
Tlr9 Agonist ◽  
Anti Inflammatory

Abstract Background and Aims The topically applied Toll-like receptor 9 [TLR9] agonist cobitolimod is a first-in-class DNA-based oligonucleotide with demonstrated therapeutic efficacy in clinical trials with ulcerative colitis [UC] patients. We here characterized its anti-inflammatory mechanism in UC. Methods Luminal cobitolimod administration was evaluated in an experimental dextran sodium sulfate [DSS]-induced colitis model. Cultured blood and mucosal cells from UC patients were treated with cobitolimod and analysed via microarray, quantitative real-time PCR, ELISA and flow cytometry. Intestinal slides of cobitolimod-treated UC patients were analysed by immunohistochemistry. Results Cobitolimod administration markedly suppressed experimental colitis activity, and microarray analyses demonstrated mucosal IL10 upregulation and suppression of IL17 signalling pathways. Cobitolimod treatment was associated with significant induction of mucosal IL10+Tr1 and Treg cells and suppression of Th17 cells. TLR9 knockout mice indicated that cobitolimod requires TLR9 signalling for IL10 induction. In UC patients, mucosal TLR9 levels correlated with severity of inflammation. Cobitolimod inhibited IL17A and IL17F, but increased IL10 and FoxP3 expression in cultured intestinal UC T cells. Cobitolimod-mediated suppression of intestinal IL17+T cells was abrogated by IL10 blockade. Furthermore, cobitolimod led to heightened IL10 production by wound healing macrophages. Immunohistochemistry in intestinal biopsies of cobitolimod-treated UC patients indicated increased presence of IL10+mononuclear and regulatory T cells, as well as reduction of IL17+cells. Conclusion Activation of TLR9 via cobitolimod might represent a novel therapeutic approach in UC, as it suppresses Th17 cells and induces anti-inflammatory IL10+macrophages and regulatory T cells, thereby modifying the dysregulated intestinal cytokine balance. Podcast This article has an associated podcast which can be accessed at https://academic.oup.com/ecco-jcc/pages/podcast

Anti-inflammatory effects of Artemisia princeps in antigen-stimulated T cells and regulatory T cells

2009 ◽  
Vol 61 (8) ◽  
pp. 1043-1050 ◽  
Author(s):  
Sung Ho Chang ◽  
Eun Jung Jung ◽  
Youn Hee Park ◽  
Dong Gyun Lim ◽  
Na Young Ko ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Artemisia Princeps ◽  
Anti Inflammatory
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