Immunological mechanisms of autoimmune gastritis

TL;DR

This paper reviews the immune mechanisms behind autoimmune gastritis, highlighting the role of both cellular and humoral immunity in disease progression.

Contribution

The paper systematically clarifies the imbalance between cellular and humoral immunity in autoimmune gastritis.

Findings

Autoimmune gastritis involves a self-attack on gastric parietal cells mediated by CD4+ T cells.

Th1/Th17 cells contribute to inflammation, while Tregs show defective suppressive function.

Current animal models have limitations in replicating T-B cell collaboration and species-specific features.

Abstract

Autoimmune gastritis (AIG) is a chronic disease characterized by specific immune damage to the gastric mucosa. Previous studies have mostly focused on the single immune pathway mainly mediated by T cells, but the synergistic role of humoral immunity in disease progression cannot be ignored. This article systematically reviews the immunological mechanism of AIG, and analyzes the inflammatory cascade immune mechanism centered on the self-attack of gastric parietal cells mediated by CD4+ T, with the pro-inflammatory roles of Th1/Th17 cells and defective suppressive function of Tregs as a supplement. This article emphasizes the imbalance between humoral and cellular immunity, including the pathogenic potential of autoantibodies and the synergistic role of T-B cells in promoting inflammation. Furthermore, while existing animal models (including genetic modification, lymphopenic, and non-lymphopenic models) can replicate features of human AIG such as gastric gland atrophy, they exhibit significant limitations regarding the mechanism of T-B cell collaboration, differences in cancer risk, and species specificity. This article systematically clarifies that AIG results from an imbalance between cellular and humoral immunity, providing a theoretical basis for targeted immunotherapy strategies.

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