Inflammatory and regulatory T cells contribute to a unique immune microenvironment in tumor tissue of colorectal cancer patients

SummarySynovial fluid from rheumatic joints displays a well-documented enrichment of forkhead box protein 3 (FoxP3)1 regulatory T cells (tissue We also demonstrate a striking enrichment of IL-1R1 expression in synovial CD4 1 T cells that was restricted to the CD25-expressing FoxP3 population, but independent of Helios. IL-1R1 expression appears to define a tissue T reg cell phenotype together with the expression of CD25, glucocorticoid-induced TNF receptor family-related gene (GITR) and CTLA-4.

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“…Such effects have also been demonstrated in other disease settings, such as type 1 diabetes and cancer [27][28][29] …”

mentioning

confidence: 78%

IL-1R1 is expressed on both Helios+ and Helios−FoxP3+CD4+ T cells in the rheumatic joint

Müller

Herrath

Malmström

2015

Clinical and Experimental Immunology

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“…Other mechanisms are probably involved in the induction of inflammatory chemokines in undifferentiated CaCo-2 cells; the inflammatory microenvironment in colorectal cancer is quite distinct from the surrounding normal tissue, allowing cancer cells to grow. Other cytokines mainly involved in immune response, such as interferon-g and IL-17, have been found very low in cultured cells from human colorectal tissue [37].…”

Section: Discussionmentioning

confidence: 99%

Evidence of cell damage induced by major components of a diet-compatible mixture of oxysterols in human colon cancer CaCo-2 cell line

et al. 2013

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a b s t r a c tCholesterol oxidation products, termed oxysterols, have been shown to be more reactive than unoxidized cholesterol, possessing marked pro-inflammatory and cytotoxic effects in a number of cells and tissues. Oxysterols, absorbed with the diet as products of cholesterol auto-oxidation, have recently been suggested to potentially interfere with homeostasis of the mucosal intestinal epithelium, by promoting and sustaining irreversible damage.However, the treatment of colon cancer cells with a diet-compatible mixture of oxysterols does not elicit the same responses than individual components added to the cells at the same concentrations at which they are present in the mixture. Sixty mM oxysterol mixture showed a slight pro-apoptotic effect on human colon cancer CaCo-2 cell line, evaluated in terms of caspase-3 and caspase-7 activation; conversely, 7a-hydroxycholesterol, 7b-hydroxycholesterol and 5a,6a-epoxycholesterol were identified to be able to induce a significant pro-apoptotic effect if added to cell culture singly; 7b-hydroxycholesterol had stronger action than other compounds. The enhanced production of reactive oxygen species through up-regulation of the colonic NADPH-oxidase isoform NOX1 appeared to be the key event in oxysterolinduced apoptosis in these colon cancer cells. As regards pro-inflammatory effects of oxysterols, IL-8 and MCP-1 were evaluated for their chemotactic activity. Only MCP-1 production was significantly induced by 7b-hydroxycholesterol, as well as by cholesterol and oxysterol mixture. However, oxysterolinduced inflammation appeared to be NOX1-independent, suggesting a secondary role of this enzyme in inducing inflammation in colon cancer cells.A selective cell death induced by specific oxysterols against colon cancer cells, mainly exploiting their ability to activate NOX1 in generating oxidative reactions, might represent a promising field of investigation in colorectal cancer, and might bring new insights on strategies in anticancer therapy.

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“…Consistently with a positive role of IL-17 in promoting tumor development, tumor tissues have a higher frequency of IL-17+ cells T cells compared with untransformed bowel tissues [28]. The protumor role of IL-17 which is mediated by inflammation-associated signaling pathways, provides additional support for the already well-established link between inflammation and tumorigenesis [29]. It has been proposed that enterotoxin producing Bacteroides fragilis (ETBF) human, colonic commensal bacterium, are able to promote colonic tumorigenesis in APC mutant mice through…”

Section: Gut Microbiota and Th17mentioning

confidence: 60%

Interplay between Gut Microbiota and T Lymphocytes in Colorectal Cancer

Hetta¹,

Elkady²,

Mekky³

et al. 2017

Colorec Cancer

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Colorectal cancer is one of the third leading causes of cancer mortality worldwide. There is increasing evidences about the involvement of gut microbiota in colorectal carcinogenesis. Several recent studies have shed light on the cross talk between gut microbiota and mucosal T cell subsets, specifically intraepithelial lymphocytes and lamina propria CD4 + T cells including T-helper cells and Tregulatory (Treg) cells which may be responsible for development of colorectal cancer through creating imbalance between proinflammatory and antiinflammatory immune cells and their cytokines. In this review, we will focus on the influence gut microbiota on the development of mucosal T cells and their role in promoting colorectal cancer.

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Inflammatory and regulatory T cells contribute to a unique immune microenvironment in tumor tissue of colorectal cancer patients

Cited by 35 publications

References 42 publications

IL-1R1 is expressed on both Helios+ and Helios−FoxP3+CD4+ T cells in the rheumatic joint

IL-1R1 is expressed on both Helios+ and Helios−FoxP3+CD4+ T cells in the rheumatic joint

Evidence of cell damage induced by major components of a diet-compatible mixture of oxysterols in human colon cancer CaCo-2 cell line

Interplay between Gut Microbiota and T Lymphocytes in Colorectal Cancer

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