ArticleInflammation2020
Mycobacterium tuberculosis Heat-Shock Protein 16.3 Induces Macrophage M2 Polarization Through CCRL2/CX3CR1.
Article in Inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- Upregulation of CREB1 by Mycobacterium Tuberculosis Transcriptionally Activates TREM2 to Promote Macrophage M2 Polarization.Cell biochemistry and function · 2026Article
- Organelle interplay in host responses and mycobacterial resilience.EMBO reports · 2026Review
- Secreted proteins ofFrontiers in tuberculosis · 2026Review
- Macrophage states and polarization duringFrontiers in cellular and infection microbiology · 2026Review
- Deciphering macrophage dynamics and immune evasion strategies by the intracellular bacteria.Immunologic research · 2025Review
- The exacerbating effects of stable pulmonary tuberculosis on the deterioration of inflammatory response, coagulation function, and pulmonary function in COPD: A propensity score-matched retrospective study.Journal of clinical tuberculosis and other mycobacterial diseases · 2025Article
- Comprehensive analysis of heat shock proteins in glioma revealed the association with glioma-associated myeloid cells.Genes and immunity · 2025Article
- Endoplasmic Reticulum Stress in Tuberculosis: Molecular Bases and Pathophysiological Implications in the Immunopathogenesis of the Disease.International journal of molecular sciences · 2025Review
- Article
- Targeting CCRL2 enhances therapeutic outcomes in a tuberculosis mouse model.Frontiers in immunology · 2025Article
- Depletion ofFrontiers in cellular and infection microbiology · 2025Article
- Transcriptomic analysis reveals TME-mediated macrophage IFIT1 upregulation and CX3CR1 suppression drive osteosarcoma progression.Frontiers in oncology · 2025Article
- Intranasal Administration of Bedaquiline-Loaded Fucosylated Liposomes Provides Anti-Tubercular Activity while Reducing the Potential for Systemic Side Effects.ACS infectious diseases · 2024Article
- Investigating the Diagnostic and Therapeutic Potential of a T Cell Receptor (TCR)-like single Domain Antibody (sDAb)-Human IgG1 Antibody against Heat Shock Protein (HSP) 16KDa/HLA-A2 for Latent Tuberculosis.Tropical medicine and infectious disease · 2024Article
- CCRL2 affects the sensitivity of myelodysplastic syndrome and secondary acute myeloid leukemia cells to azacitidine.Haematologica · 2023Article
- Bacteria and macrophages in the tumor microenvironment.Frontiers in microbiology · 2023Review
- Early innate cell interactions withFrontiers in immunology · 2023Review
- Review
- Macrophage: A Cell With Many Faces and Functions in Tuberculosis.Frontiers in immunology · 2022Review
- Understanding Metabolic Regulation Between Host and Pathogens: New Opportunities for the Development of Improved Therapeutic Strategies AgainstFrontiers in cellular and infection microbiology · 2021Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Mycobacterium tuberculosis, the pathogen of tuberculosis (TB), can survive in host macrophages and induce macrophages to M2 phenotype might result in latent MTB infection. During the latent phase, the expression of MTB heat-shock protein 16.3 (Hsp16.3) is markedly increased among most of bacterial proteins, but the role of Hsp16.3 in macrophage M2 polarization is not clear. In this work, we found that macrophages incubated with 100 ng/ml MTB Hsp16.3 increased the production of Arg-1, IL-10, TGF-beta, and CD206. These results showed that MTB Hsp16.3 may induce macrophage M2 phenotype. And the interaction of Hsp16.3 with macrophages was found to depend on chemokine receptors CCRL2 and CX3CR1. Additionally, we used overexpression and silencing techniques to further verify the effect of CCRL2 and CX3CR1 on MTB Hsp16.3-induced M2 polarization macrophages. Furthermore, we explored the downstream signaling molecules of CCRL2 and CX3CR1 and we found MTB Hsp16.3 altered the signal transduction of the AKT/ERK/p38-MAPK. Taken together, this study provides evidence that MTB Hsp16.3 promotes macrophages to M2 phenotype and explores its underlying mechanism.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.