Increased infiltration of CD4+ IL-17A+ FOXP3+ T cells in Helicobacter pylori-induced gastritis.
Eur J Immunol
; 54(3): e2350662, 2024 Mar.
Article
in En
| MEDLINE
| ID: mdl-38366919
ABSTRACT
Helicobacter pylori is one of the main predisposing factors for gastric cancer, causing chronic inflammation and proper glands atrophy in the gastric mucosa. Although H. pylori-induced inflammation is a key inducer of precancerous lesions in the gastric mucosa, it remains unclear which precise immune cell subsets are responsible for the progression of H. pylori-induced gastritis. Here, we observed an abundance of CD4+ IL-17A+ FOXP3+ T cells exhibiting a Th17-like phenotype within the microenvironment of H. pylori-induced gastritis. Mechanistically, H. pylori upregulated the expression of IL-6 in Dendritic cells and macrophages, by activating NF-κB signaling through the virulence factor CagA and thus, induced IL-17A expression in FOXP3+ T cells. Moreover, CD4+ IL-17A+ FOXP3+ T cells were positively associated with advanced precancerous lesions. Therefore, these findings offer essential insights into how FOXP3+ T cells sense inflammatory signals from the environment, such as IL-6, during H. pylori infections, thereby guiding the effector immune response and aggravating the gastritis.
Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Precancerous Conditions
/
Helicobacter pylori
/
Helicobacter Infections
/
Gastritis
Limits:
Humans
Language:
En
Journal:
Eur J Immunol
Year:
2024
Document type:
Article
Affiliation country:
Country of publication: