scholarly journals From 'perfect mix' to 'potion magique' — regulatory T cells and anti-inflammatory cytokines as adjuvant targets

2008 ◽  
Vol 6 (1) ◽  
pp. 88-88 ◽  
Author(s):  
Jagadeesh Bayry ◽  
Darren R. Flower ◽  
David F. Tough ◽  
Srini V. Kaveri
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Inflammatory Cytokines ◽  
Anti Inflammatory

The influence of sex hormones on cytokines in multiple sclerosis and experimental autoimmune encephalomyelitis: a review

2005 ◽  
Vol 11 (3) ◽  
pp. 349-359 ◽  
Author(s):  
Hans HLP van den Broek ◽  
Jan GMC Damoiseaux ◽  
Marc H De Baets ◽  
Raymond MM Hupperts
Keyword(s):  
Multiple Sclerosis ◽  
Immune Response ◽  
T Cells ◽  
Regulatory T Cells ◽  
Sex Hormones ◽  
Inflammatory Cytokines ◽  
Cytokine Production ◽  
Anti Inflammatory ◽  
Experimental Autoimmune

The female predominance of multiple sclerosis (MS) has suggested that hormonal differences between the sexes must confer some protective effect on males or enhance the susceptibility of females to this disease. There has been evidence that gonadal hormones can modulate the immune response regulated by antigen presenting cells and T cells. These cells control the immune response by the production of interacting pro- and anti-inflammatory cytokines. The first include the acute phase pro-inflammatory cytokines of the innate immune response as well as the T-helper 1 (Th1) cytokines, while the later contain the Th2 cytokines as well as the suppressor cytokines. There is some evidence that MS and experimental autoimmune encephalitis (EAE) are Th1 cell-mediated diseases. For this reason many studies have been done to influence the pro-inflammatory cytokine production of these Th1 cells in favour of an anti-inflammatory immune response as mediated by Th2 cells. However the role of the regulatory T cells in this context is not clearly understood. Here we review the studies concerning the role of sex hormones on the cytokine production in relation to the disease course of MS and EAE and in particular in the light of the recent revival of the regulatory T cells and their suppressive cytokines.

scholarly journals Human Wharton’s Jelly Mesenchymal Stem Cell-Mediated Sciatic Nerve Recovery Is Associated with the Upregulation of Regulatory T Cells

2020 ◽  
Vol 21 (17) ◽  
pp. 6310
Author(s):  
Aline Yen Ling Wang ◽  
Charles Yuen Yung Loh ◽  
Hsin-Hsin Shen ◽  
Sing-Ying Hsieh ◽  
Ing-Kae Wang ◽  
...  
Keyword(s):  
T Cells ◽  
Sciatic Nerve ◽  
Regulatory T Cells ◽  
Inflammatory Cytokines ◽  
Peripheral Nerve Regeneration ◽  
Wharton’S Jelly ◽  
Treg Depletion ◽  
Wharton's Jelly ◽  
Nerve Recovery ◽  
Anti Inflammatory

The acceleration of peripheral nerve regeneration is crucial for functional nerve recovery. Our previous study demonstrated that human Wharton’s jelly-derived mesenchymal stem cells (hWJ-MSC) promote sciatic nerve recovery and regeneration via the direct upregulation and release of neurotrophic factors. However, the immunomodulatory role of hWJ-MSC in sciatic nerve recovery remains unclear. The effects of hWJ-MSC on innate immunity, represented by macrophages, natural killer cells, and dendritic cells, as well as on adaptive immunity, represented by CD4+ T, CD8+ T, B, and regulatory T cells (Tregs), were examined using flow cytometry. Interestingly, a significantly increased level of Tregs was detected in blood, lymph nodes (LNs), and nerve-infiltrating cells on POD7, 15, 21, and 35. Anti-inflammatory cytokines, such as IL-4 and IL-10, were significantly upregulated in the LNs and nerves of hWJ-MSC-treated mice. Treg depletion neutralized the improved effects of hWJ-MSC on sciatic nerve recovery. In contrast, Treg administration promoted the functional recovery of five-toe spread and gait stance. hWJ-MSC also expressed high levels of the anti-inflammatory cytokines TGF-β and IL-35. This study indicated that hWJ-MSC induce Treg development to modulate the balance between pro- and anti-inflammation at the injured sciatic nerve by secreting higher levels of anti-inflammatory cytokines.

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 Selective expansion of memory CD4+ T cells by mitogenic human CD28 generates inflammatory cytokines and regulatory T cells

2008 ◽  
Vol 38 (6) ◽  
pp. 1522-1532 ◽  
Author(s):  
Manisha Singh ◽  
Sreemanti Basu ◽  
Christina Camell ◽  
Jacob Couturier ◽  
Rodolfo J. Nudelman ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Inflammatory Cytokines ◽  
Cd4 T Cells ◽  
Memory Cd4 T Cells

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

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