Immune Biology and Persistence of Helicobacter pylori in Gastric Diseases.

Helicobacter pylori is a prevalent pathogen, which affects more than 40% of the global population. It colonizes the human stomach and persists in its host for several decades or even a lifetime, if left untreated. The persistent infection has been linked to various gastric diseases, including gastritis, peptic ulcers, and an increased risk for gastric cancer.

CagA-specific Gastric CD8 Tissue-Resident T Cells Control Helicobacter pylori During the Early Infection Phase.

Background & Aims: Infection with Helicobacter pylori strongly affects global health by causing chronic gastritis, ulcer disease, and gastric cancer. Although extensive research into the strong immune response against this persistently colonizing bacterium exists, the specific role of CD8 T cells remains elusive.

Methods: We comprehensively characterize gastric H pylori-specific CD8 T-cell responses in mice and humans by flow cytometry, RNA-sequencing, immunohistochemistry, and ChipCytometry, applying functional analyses including T-cell depletion, H pylori eradication, and ex vivo restimulation.

Genome-Wide ChIP-seq and RNA-seq Analyses of STAT3 Target Genes in TLRs Activated Human Peripheral Blood B Cells.

Toll like receptors (TLRs) induced response plays a vital role in B-cell development and activation, in which TLR7-mediated and TLR9-mediated response interact together and play antagonistic or cooperative roles at different situations. Previous studies showed that the transcription factor signal transducer and activator of transcription (STAT) 3 was one of the key transcriptional factors (TFs) needed for both TLR7 and TLR9 signaling in B cell, and patients with autosomal dominant hyper IgE syndromes (AD-HIES) due to mutations having defective TLRs response in B cells. However, how STAT3 affects its target genes and the downstream signaling pathways in B cell upon TLRs stimulation remains unclarified on a genome-wide level.

Defective Toll-Like Receptors Driven B Cell Response in Hyper IgE Syndrome Patients With Mutations.

Autosomal dominant hyper-IgE syndrome (AD-HIES) is a rare inherited primary immunodeficient disease (PIDs), which is caused by gene mutations. Previous studies indicated a defective Toll-like receptor (TLR) 9-induced B cell response in AD-HIES patients, including proliferation, and IgG production. However, the other TLRs-mediated B cell responses in AD-HIES patients were not fully elucidated.

A Biodegradable Mg-Based Alloy Inhibited the Inflammatory Response of THP-1 Cell-Derived Macrophages Through the TRPM7-PI3K-AKT1 Signaling Axis.

Mg-based alloys might be ideal biomaterials in clinical applications owing to favorable mechanical properties, biodegradability, biocompatibility, and especially their anti-inflammatory properties. However, the precise signaling mechanism underlying the inhibition of inflammation by Mg-based alloys has not been elucidated. Here, we investigated the effects of a Mg-2.

Immunoregulatory effect of human β-defensin 1 on neonatal cord blood monocyte-derived dendritic cells and T cells.

The relationship between breastfeeding and infant health has been well elucidated in past decades. Our previous study has shown that human β-defensin 1 (hBD-1) in human breast milk plays a protective role in reducing the incidence of upper respiratory infection in infants younger than 6 months. In the present study, we aim to reveal the mechanism underlying the protective role of hBD-1 by focusing on its immunoregulatory function in neonates.

Degradation Products of Polydopamine Restrained Inflammatory Response of LPS-Stimulated Macrophages Through Mediation TLR-4-MYD88 Dependent Signaling Pathways by Antioxidant.

Polydopamine (PDA) has a promising application as coating of biomaterials due to its favorable degradability and bioadaptability. However, its bioactivity, such as anti-inflammatory capacity, was still little known. Herein, we investigated whether degradable products of PDA could affect inflammatory response in lipopolysaccharide (LPS)-stimulated human THP-1-derived macrophages.

Clinical, Laboratory, and Molecular Characteristics and Remission Status in Children With Severe Congenital and Non-congenital Neutropenia.

Severe congenital neutropenia (SCN) is a primary immunodeficiency disease characterized by the early onset of recurrent infections and persistent severe neutropenia, with or without genetic defect. We aimed to study the different clinical features and hematological and bone marrow characteristics of patients with SCN and the non-congenital form of severe neutropenia (SN) with unknown etiology. Thirty-nine Chinese children with severe neutropenia for longer than 6 months unrelated to virus infection or autoimmune diseases were enrolled in the study to analyse the clinical, laboratory, and molecular characteristics.

Clinical Manifestations and Genetic Analysis of 17 Patients with Autosomal Dominant Hyper-IgE Syndrome in Mainland China: New Reports and a Literature Review.

Purpose: Autosomal dominant hyper-IgE syndrome (AD-HIES) is a rare complicated primary immunodeficiency disease (PID). Signal transducer and activator of transcription 3 (STAT3) gene mutation is found to cause AD-HIES. The distribution of AD-HIES patients with STAT3 deficiency in the Chinese population is not clear.