What question did this study set out to answer?

This research aims to understand how H. pylori influences macrophage activation and impairs the adaptive immune response.

August 13, 2026Archives of MicrobiologyOpen Access

Helicobacter pylori promote M1 macrophage polarization via JAK3-mediated activation of the SOCS3/IL2RA axis to suppress host immunity

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Randomized trial shows JAK3-mediated immune effects in macrophages, highlighting potential interventions for chronic gastritis.

This research aims to understand how H. pylori influences macrophage activation and impairs the adaptive immune response.
Infected RAW264.7 macrophages with H. pylori PMSS1 to analyze polarization and cytokine levels.
Used Ritlecitinib to inhibit JAK3 and assessed its effects on inflammatory gene expression.
Evaluated T-cell responses to macrophage-conditioned medium in primary naive CD4⁺ T cells.
H. pylori significantly promoted M1 macrophage polarization, indicated by elevated levels of CD86, iNOS, and TNF-α (p < 0.05).
Primary CD4⁺ T-cell activation and proliferation were inhibited by macrophage-conditioned medium (p < 0.05).
SOCS3 knockdown partially restored T-cell responses, implying its role in immune suppression (p < 0.05).

Chen et al. (2026) studied this question.

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August 13, 2026Archives of MicrobiologyOpen Access

View Full Paper

Ask AI

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Authors

Randomized trial shows JAK3-mediated immune effects in macrophages, highlighting potential interventions for chronic gastritis.

This research aims to understand how H. pylori influences macrophage activation and impairs the adaptive immune response.
Infected RAW264.7 macrophages with H. pylori PMSS1 to analyze polarization and cytokine levels.
Used Ritlecitinib to inhibit JAK3 and assessed its effects on inflammatory gene expression.
Evaluated T-cell responses to macrophage-conditioned medium in primary naive CD4⁺ T cells.
H. pylori significantly promoted M1 macrophage polarization, indicated by elevated levels of CD86, iNOS, and TNF-α (p < 0.05).
Primary CD4⁺ T-cell activation and proliferation were inhibited by macrophage-conditioned medium (p < 0.05).
SOCS3 knockdown partially restored T-cell responses, implying its role in immune suppression (p < 0.05).

Chen et al. (2026) studied this question.

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