Pathogenetic mechanisms in AIG (2022, Clinical and Translational Gastroenterology) : 대한자가면역성위염연구회

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2022-11-20

Summary of the potential pathogenetic mechanisms in autoimmune atrophic gastritis (AAG), according to the results found in the study. The oxyntic glands are made of different cell types including epithelial cells (e.g., mucous neck cells and chief cells) and parietal cells. The H+/K+ ATPase can be found on parietal cells, and its beta subunit constitutes the major autoantigen recognized by the T-cell receptor (TCR) located on T cells, through the major histocompatibility complex (MHC) II. Subsequently, autoreactive CD4+ T cells produce tumor necrosis factor (TNF)-α, interleukin (IL)-33, and IL-15, all promoting a cascade which determines epithelial cell apoptosis and atrophy. In addition, autoreactive T cells also stimulate B cells that differentiate into plasma cells producing anti-parietal cell antibodies (PCAs) and anti-intrinsic factor antibodies (IFAs). Transforming growth factor (TGF)-β1 is also produced by T cells; it stimulates different lamina propria mononuclear cells (LPMCs) that in turn release matrix metalloproteinase 3 (MMP3), favoring fibrosis and tissue remodeling. Intracellular nicotinamide phosphoribosyltransferase (iNAMPT) is released by LPMCs and, in the form of extracellular NAMPT (eNAMPT), further enhances the B-cell immune response. The whole inflammatory process may potentially be counteracted by thymic stromal lymphopoietin (TSLP), which is produced by epithelial cells, acting on the TSLP receptor (TSLPR) located on T cells. Finally, the reduced expression of plasmalemma vesicle 1 (PV1) may lead to a lower gastric vascular permeability, maybe as a consequence of hypo‐achlorhydria that favors bacterial overgrowth.

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