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Updated: Jun 27, 2025

Polarization of M1 and M2 Human Monocyte-Derived Cells and Analysis with Flow Cytometry upon Mycobacterium tuberculosis Infection
Published on: September 18, 2020
M2 macrophages participate in ILC2 activation induced by Helicobacter pylori infection
Ruyi Peng1,2,3, Canxia Xu4,5, Linfang Zhang6
1Department of Gastroenterology, the Second Xiangya Hospital of Central South University, Changsha, Hunan Province, China.
Abstract:
Helicobacter pylori (H. pylori) causes a diversity of gastric diseases. The host immune response evoked by H. pylori infection is complicated and can influence the development and progression of diseases. We have reported that the Group 2 innate lymphocytes (ILC2) were promoted and took part in building type-2 immunity in H. pylori infection-related gastric diseases. Therefore, in the present study, we aim to clarify how H. pylori infection induces the activation of ILC2. It was found that macrophages were necessary for activating ILC2 in H. pylori infection. Mechanistically, H. pylori infection up-regulated the expression of indoleamine 2,3-dioxygenase (IDO) in macrophages to induce M2 polarization, and the latter secreted the alarmin cytokine Thymic Stromal Lymphopoietin (TSLP) to arouse ILC2.
Insights
Helicobacter pylori infection activates Group 2 innate lymphocytes (ILC2) via macrophages. Macrophages upregulate indoleamine 2,3-dioxygenase (IDO), promoting M2 polarization and Thymic Stromal Lymphopoietin (TSLP) secretion, which then activates ILC2.
Area of Science:
- Immunology
- Gastroenterology
- Microbiology
Background:
- Helicobacter pylori infection is linked to various gastric diseases.
- Host immune responses, particularly type-2 immunity involving Group 2 innate lymphocytes (ILC2), play a role in disease progression.
- The precise mechanisms by which H. pylori infection activates ILC2 remain unclear.
Purpose of the Study:
- To elucidate the mechanism by which H. pylori infection induces ILC2 activation.
- To investigate the role of macrophages in H. pylori-induced ILC2 responses.
- To identify key molecular mediators involved in this immune crosstalk.
Main Methods:
- Utilized a mouse model of H. pylori infection.
- Analyzed macrophage activation and polarization.
- Assessed ILC2 populations and activation markers.
- Measured indoleamine 2,3-dioxygenase (IDO) and Thymic Stromal Lymphopoietin (TSLP) expression.
Main Results:
- Macrophages were identified as essential for H. pylori-induced ILC2 activation.
- H. pylori infection upregulated IDO expression in macrophages, driving M2 polarization.
- M2-polarized macrophages secreted TSLP, a crucial cytokine for ILC2 activation.
- This pathway contributes to type-2 immunity during H. pylori infection.
Conclusions:
- H. pylori infection activates ILC2 through a macrophage-dependent pathway.
- IDO-mediated M2 polarization of macrophages and subsequent TSLP secretion are critical steps.
- Understanding this mechanism offers insights into H. pylori-related gastric pathology and potential therapeutic targets.
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