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. 2021 Apr 28;13(5):315. doi: 10.3390/toxins13050315

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Illustration of immune cellular interaction in H. pylori infection. H. pylori is sensed by dendritic cell (DCs) and epithelial cells followed by the advent of CD4⁺ T cells, PMN, and macrophage to the gastric mucosa for bacterial clearance. However, continuous activation might increase local inflammation. Bacteria could modulate the escape mechanism and skew DCs to produce IL-23. Th17 equilibrium leans to the pathogenic side, along with Th1 releasing proinflammatory cytokines that recruit more PMNs. Regulatory T cells reportedly suppress the inflammatory effects of infection in the gastric mucosa. Treg, regulatory T cell; Th1, T helper produce IFNγ; Th17, T helper produce IL-17; DC, dendritic cell; Mϕ, macrophage; PMN, polymononuclear neutrophil; B cell, lymphocyte produce antibody.