Human CD4+ T-cell receptor recognizing Helicobacter pylori antigens (H. pylori-specific CD4+ TCR)

Human CD4+ T-cell receptors (TCRs) specific for Helicobacter pylori antigens, including CagA, VacA, and NAP, are central mediators of the adaptive immune response to this chronic gastric pathogen. These TCRs recognize specific peptide epitopes derived from H. pylori virulence factors when they are presented by Major Histocompatibility Complex class II (MHC II) molecules, primarily HLA-DR, on antigen-presenting cells [1][2]. CagA is an oncoprotein that disrupts host cell signaling, VacA is a toxin that induces cellular vacuolation and apoptosis, and NAP is a potent stimulator of neutrophil recruitment and activation [3][4]. Upon binding to these peptide-MHC complexes, the TCRs initiate signaling cascades that lead to the differentiation of CD4+ T cells into Th1 and Th17 effector subsets, which secrete cytokines such as interferon-gamma (IFN-g) and interleukin-17 (IL-17) [5]. While this response is intended to clear the infection, the persistent nature of H. pylori often leads to a chronic inflammatory state that increases the risk of peptic ulcers and gastric adenocarcinoma [6]. These TCRs are considered therapeutic targets for the development of precision vaccines and TCR-engineered T-cell therapies designed to enhance protective immunity or modulate the pathological inflammatory response [7].

Other names

H. pylori-specific T-cell receptorCagA/VacA/NAP-specific CD4+ TCRHelicobacter pylori-reactive T-cell receptor

Recognition of Helicobacter pylori peptides (CagA, VacA, and NAP) presented on MHC Class II molecules, leading to CD4+ T-cell activation and pro-inflammatory cytokine release.