H. pylori modulates DC functions via T4SS/TNFα/p38-dependent SOCS3 expression.

ABSTRACT:

Background

Helicobacter pylori (H. pylori) is a gram-negative bacterium that chronically infects approximately 50% of the world's human population. While in most cases the infection remains asymptomatic, 10% of infected individuals develop gastric pathologies and 1-3% progress to gastric cancer. Although H. pylori induces severe inflammatory responses, the host's immune system fails to clear the pathogen and H. pylori can persist in the human stomach for decades. As suppressor of cytokine signaling (SOCS) proteins are important feedback regulators limiting inflammatory responses, we hypothesized that H. pylori could modulate the host's immune responses by inducing SOCS expression.

Methods

The phenotype of human monocyte-derived DCs (moDCs) infected with H. pylori was analyze

SUBMITTER: Sarajlic M 

PROVIDER: S-EPMC7541176 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature