CD4+ regulatory T cells in gastric cancer mucosa are proliferating and express high levels of IL-10 but little TGF-β

Kindlund, Bert; Sjöling, Åsa; Yakkala, Chakradhar; Adamsson, Jenni; Janzon, Anders; Hansson, Lars‐Erik; Hermansson, Michael; Janson, Peter; Winqvist, Ola; Lundin, Samuel

doi:10.1007/s10120-015-0591-z

Cited by 69 publications

(59 citation statements)

References 56 publications

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“…In addition, gastric tissues of the infection group contained more Foxp3(+) cells, indicating a role of Treg in H. pylori ‐induced pathologies. The hypothesized mechanism of H. pylori ‐induced Treg to promote tumor growth by modulating the antitumor immune response has also been addressed by Kindlund et al . They demonstrated proliferation of CD4+ FOXP3+ CD25 high Treg in the stomach mucosa of patients with gastric cancer.…”

Section: Adaptive Immune Responsementioning

confidence: 97%

Inflammation, immunity, and vaccines for Helicobacter pylori infection

Velin

Straubinger²,

Gerhard

2016

Helicobacter

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The tight control of the innate and adaptive immune responses in the stomach mucosa during chronic Helicobacter pylori infection is of prime importance for the bacteria to persist and for the host to prevent inflammation-driven diseases. This review summarizes recent data on the roles of innate and adaptive immune responses during H. pylori/host interactions. In addition, the latest preclinical developments of H. pylori vaccines are discussed with a special focus on the clinical trial reported by Zeng et al., who provided evidence that oral vaccination significantly reduces the acquisition of natural H. pylori infection in children.

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Section: Adaptive Immune Responsementioning

confidence: 97%

Inflammation, immunity, and vaccines for Helicobacter pylori infection

Velin

Straubinger²,

Gerhard

2016

Helicobacter

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“…It was observed that CD4 + FOXP3 + T cells within GC tissue are more abundant than CD4 + FOXP3 -T cells. CD4 + CD25 high T cells present higher expression of 10/IFN-γ gene and lowered TGF-β levels [229]. observed that smaller tumor size correlates with higher expression of peripheral CD4+ and CD8+ cells [230].…”

Section: Lymphocytesmentioning

confidence: 99%

Immunological Aspects of the Tumor Microenvironment and Epithelial-Mesenchymal Transition in Gastric Carcinogenesis

Baj

Brzozowska

Forma

et al. 2020

IJMS

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Infection with Helicobacter pylori, a Gram-negative, microaerophilic pathogen often results in gastric cancer in a subset of affected individuals. This explains why H. pylori is the only bacterium classified as a class I carcinogen by the World Health Organization. Several studies have pinpointed mechanisms by which H. pylori alters signaling pathways in the host cell to cause diseases. In this article, the authors have reviewed 234 studies conducted over a span of 18 years (2002)(2003)(2004)(2005)(2006)(2007)(2008)(2009)(2010)(2011)(2012)(2013)(2014)(2015)(2016)(2017)(2018)(2019)(2020). The studies investigated the various mechanisms associated with gastric cancer induction. For the past 1.5 years, researchers have discovered new mechanisms contributing to gastric cancer linked to H. pylori etiology. Alongside alteration of the host signaling pathways using oncogenic CagA pathways, H. pylori induce DNA damage in the host and alter the methylation of DNA as a means of perturbing downstream signaling. Also, with H. pylori, several pathways in the host cell are activated, resulting in epithelial-to-mesenchymal transition (EMT), together with the induction of cell proliferation and survival. Studies have shown that H. pylori enhances gastric carcinogenesis via a multifactorial approach. What is intriguing is that most of the targeted mechanisms and pathways appear common with various forms of cancer.EMT refers to the process by which the mesenchymal phenotype is acquired by epithelial cells (ECs) mainly via the reduction of their intracellular adhesions and proliferative capacity (Figure 1.) [47].

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“…The inhibition of CCL2 by apigenin occurred through suppression of IKBKe signalling. [163][164][165][166][167][168][169][170][171][172] Apigenin overcame drug resistance and decreased colonization and cell growth in adriamycinresistant MCF-7 cells via downregulation of MDR1 and Pglycoprotein, as well as, suppression of STAT3 signalling and its nuclear translocation. The compound also diminished the secretion of MMP-9 and VEGF (STAT3 target genes) in these cells.…”

Section: Apigeninmentioning

confidence: 99%

Mechanistic evaluation of phytochemicals in breast cancer remedy: current understanding and future perspectives

et al. 2018

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CD4+ regulatory T cells in gastric cancer mucosa are proliferating and express high levels of IL-10 but little TGF-β

Abstract: Background An increase of regulatory T cells, defined as CD25 high -and/or FOXP3

Cited by 69 publications

References 56 publications

Inflammation, immunity, and vaccines for Helicobacter pylori infection

Inflammation, immunity, and vaccines for Helicobacter pylori infection

Immunological Aspects of the Tumor Microenvironment and Epithelial-Mesenchymal Transition in Gastric Carcinogenesis

Mechanistic evaluation of phytochemicals in breast cancer remedy: current understanding and future perspectives

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