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Review
. 2022 May 23:13:899161.
doi: 10.3389/fimmu.2022.899161. eCollection 2022.

The Efficacy of Cancer Immunotherapies Is Compromised by Helicobacter pylori Infection

Paul Oster  1 , Laurie Vaillant  1 , Brynn McMillan  1 , Dominique Velin  1
Affiliations
Review

The Efficacy of Cancer Immunotherapies Is Compromised by Helicobacter pylori Infection

Paul Oster et al. Front Immunol. .

Erratum in

Abstract

Helicobacter pylori infects the gastric mucosa of a large number of humans. Although asymptomatic in the vast majority of cases, H pylori infection can lead to the development of peptic ulcers gastric adenocarcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma. Using a variety of mechanisms, H pylori locally suppresses the function of the host immune system to establish chronic infection. Systemic immunomodulation has been observed in both clinical and pre-clinical studies, which have demonstrated that H pylori infection is associated with reduced incidence of inflammatory diseases, such as asthma and Crohn's disease. The introduction of immunotherapies in the arsenal of anti-cancer drugs has revealed a new facet of H pylori-induced immune suppression. In this review, we will describe the intimate interactions between H pylori and its host, and formulate hypothtyeses describing the detrimental impact of H pylori infection on the efficacy of cancer immunotherapies.

Keywords: Helicobacter pylori; cancer; gut microbiota; immune checkpoint inhibitors; immunotherapy; personalized medicine.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
H pylori infection modulates the activity of macrophages, dendritic cells and T lymphocytes. (A) When in contact with H pylori, cytotoxin-associated gene A (CagA) and/or urease, skew macrophages toward an M2 phenotype, which promotes Treg cell differentiation, inhibits CD8+ T cell responses and/or promotes apoptosis. (B) H pylori, CagA, γ-glutamyl transpeptidase (γGT), vacuolating cytotoxin A (VacA), Lipopolysaccharide (LPS), glutamate and urease trigger the differentiation of tolerogenic DCs, leading to the Treg cell-skewed Th response. (C) γGT, VacA and Arginase inhibit the proliferation of CD4+ and CD8+ T cells.
Figure 2
Figure 2
Local and remote effects of H pylori infection on host immune functions. In the gastric mucosa, H pylori promotes the differentiation of tolerogenic DCs, M2 macrophages, Treg cells, inhibits Th1/Th17 responses and/or sequesters CD8+ T cells. The systemic diffusion/migration of extracellular vesicles, outer membrane vesicles (OMVs), Treg cells, tolerogenic DCs and M2 macrophages modulates the function of primary and secondary lymphoid organs, leading to a decrease in tumor specific immune responses triggered by cancer immunotherapies.
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