ArticleMediators of inflammation2022
M2c Macrophages Protect Mice from Adriamycin-Induced Nephropathy by Upregulating CD62L in Tregs.
Article in Mediators of inflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Tetrahydropalmatine may alleviate doxorubicin-induced renal injury by activating the Sirt3-mediated Nrf2/HO-1 pathway.Biology direct · 2026Article
- Emerging therapeutic pipelines on kidney fibrosis: challenges in translational research.Journal of translational medicine · 2026Review
- Mendelian Randomization and Experimental Validation Identify Key Immune Signatures in Bullous Pemphigoid.Clinical, cosmetic and investigational dermatology · 2026Article
- A novel model for predicting the risk of liver cirrhosis in people living with HIV/HBV coinfection: a study based on proteomic analysis.BMC infectious diseases · 2025Article
- Innate immune cells in acute and chronic kidney disease.Nature reviews. Nephrology · 2025Review
- Macrophage expression of constitutively activeHeliyon · 2025Article
- Histone modifications and metabolic reprogramming in tumor-associated macrophages: a potential target of tumor immunotherapy.Frontiers in immunology · 2025Review
- Revisiting regulatory T cells as modulators of innate immune response and inflammatory diseases.Frontiers in immunology · 2023Review
- Single-Cell RNA Sequencing and Transcriptome Analysis Revealed the Immune Microenvironment and Gene Markers of Acute Respiratory Distress Syndrome.Journal of inflammation research · 2023Article
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Authors and funding
9 authors.
Funding
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Abstract
Regulatory T cells (Tregs) and M2c macrophages have been shown to exert potentially synergistic therapeutic effects in animals with adriamycin-induced nephropathy (AN), a model chronic proteinuric renal disease. M2c macrophages may protect against renal injury by promoting an increase in the number of Tregs in the renal draining lymph nodes of AN mice, but how they do so is unclear. In this study, we used an AN mouse model to analyze how M2c macrophages induce the migration of Tregs. Using flow cytometry, we found that M2c macrophages promoted the migration of Tregs from the peripheral blood to the spleen, thymus, kidney, and renal draining lymph nodes. At the same time, M2c macrophages significantly upregulated chemokine receptors and adhesion molecule in Tregs, including CCR4, CCR5, CCR7, CXCR5, and CD62L. Treating AN mice with monoclonal anti-CD62L antibody inhibited the migration of M2c macrophages and Tregs to the spleen, thymus, kidney, and renal draining lymph nodes. Taken together, our results suggest that M2c macrophages upregulate CD62L in Tregs and thereby promote their migration to inflammatory sites, where they exert renoprotective effects. These insights may aid the development of treatments against chronic kidney disease.
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