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Updated: Aug 24, 2025
Depletion and Reconstitution of Macrophages in Mice
Published on: August 1, 2012
M2c Macrophages Protect Mice from Adriamycin-Induced Nephropathy by Upregulating CD62L in Tregs
Junyu Lu1, Shengqiu Lv1, Jielong Pang2
1Intensive Care Unit, The Second Affiliated Hospital of Guangxi Medical University, Nanning, China.
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.
Insights
M2c macrophages enhance kidney protection by upregulating CD62L in regulatory T cells (Tregs), promoting their migration to inflammatory sites. This mechanism offers insights for treating chronic kidney disease.
Area of Science:
- Immunology
- Nephrology
- Cell Biology
Background:
- Regulatory T cells (Tregs) and M2c macrophages show therapeutic potential in adriamycin-induced nephropathy (AN).
- M2c macrophages may protect kidneys by increasing Treg numbers in renal draining lymph nodes, but the mechanism is unknown.
Purpose of the Study:
- To investigate the mechanism by which M2c macrophages induce Treg migration in a mouse model of chronic kidney disease.
Main Methods:
- Utilized an adriamycin-induced nephropathy (AN) mouse model.
- Employed flow cytometry to analyze Treg migration and chemokine receptor/adhesion molecule expression.
- Administered anti-CD62L antibody to assess its impact on cell migration.
Main Results:
- M2c macrophages promoted Treg migration from blood to spleen, thymus, kidney, and lymph nodes.
- M2c macrophages upregulated CCR4, CCR5, CCR7, CXCR5, and CD62L in Tregs.
- Anti-CD62L antibody treatment inhibited M2c macrophage and Treg migration to key organs.
Conclusions:
- M2c macrophages upregulate CD62L on Tregs, facilitating their migration to inflammatory sites for renoprotective effects.
- This study elucidates a novel mechanism for M2c macrophage-mediated Treg recruitment in kidney disease.
- Findings may inform the development of novel therapies for chronic kidney disease.
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