Monocyte Depletion & Macrophage

Monocyte depletion refers to the reduction or elimination of monocytes, which are precursor cells to macrophages, from the bloodstream or tissues. The depletion of monocytes can have downstream effects on macrophage populations and functions, as monocytes are a primary source of tissue-resident macrophages under steady-state conditions and contribute to the replenishment of macrophage populations in response to inflammation or injury. Monocyte depletion affects macrophages in several ways:

• Reduction in Macrophage Recruitment
• Altered Macrophage Phenotype
• Impaired Tissue Repair and Homeostasis
• Modulation of Immune Responses

Tissue-specific macrophage blocking technology based on monocyte depletion is a completely new area of research. As a team of researchers who continue to explore and discover macrophages, Creative Biolabs is committed to being at the forefront of science, bringing complete design ideas and reliable data results to your research.

Our Service

Understanding the consequences of monocyte depletion on macrophage biology is essential for elucidating the roles of these cells in health and disease and for developing therapeutic strategies targeting macrophage-mediated pathologies. Creative Biolabs offers a range of tissue-specific macrophage-based blocking services based on monocyte depletion to accelerate your scientific research, including but not limited to:

• ELISA, Immunofluorescence, flow cytometry, western blot
• Monocyte depletion mouse model
• Bulk RNA-seq: sample preparation and analysis
• Single-cell RNA sequencing and analysis
• Single-cell RNA velocity estimation
• Gene Ontology enrichment analysis

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Published Data

• Background

Most of the cells that make up the human body come from stem cells, which are constantly dividing to produce more cells. Studies have found that this ability to proliferate is not limited to stem cells, but also monocytes in the blood. Monocytes are able to proliferate locally and then differentiate into different subsets of mesenchymal macrophages. This study validates the ability of monocytes to proliferate in an empty niche in a manner restricted by MafB and then differentiate into distinct mesenchymal macrophage subpopulations.

• Here are some of the key results from this study:

Trajectory from monocytes to interstitial macrophages.
Fig.1 scRNA-seq analysis reveals different transitional cells.1	Single-cell RNA sequencing (scRNA-seq) analysis was performed for monocytes and mesenchymal macrophages sorted from IMDTR mice. Based on differential expression analysis, cell clusters corresponding to different cells were identified, including cMo (C1), pMo (C2), CD206- IM (C3), and CD206+ IM (C4), while C6 represented transitional monocytes (Tr-Mo). RNA rate analysis also showed that Tr-Mo was moving from cMo to IM subsets. These experiments captured the complete trajectory from monocytes to mesenchymal macrophages at the single-cell transcriptome level.
Transitional monocytes proliferate locally in a Csf1r-dependent manner.
Fig.2 Trajectory analysis of mesenchymal macrophage development identifies transiently proliferating monocytes.1	Monocle single-cell trajectory analysis was then performed and two main trajectories were found. They all start from cMo, cross Tr-Mo to the fork point, and then fork towards CD206- IM or CD206+ IM. In addition, genes associated with cell proliferation (e.g., Ube2c, Aurkb, Racgap1, Cdk1, etc.) were also observed to be upregulated, corresponding to increased S and G2/M cell cycle scores for Tr-Mo, indicating the presence of DNA replication and mitosis. By plotting quasi-temporal maps of cMo features, S phase and G2/M phases, and IM features, it was found that cMo becomes Tr-Mo once it enters an empty niche, then re-enters the cell cycle and expands, and finally differentiates into CD206- IM or CD206+ IM.
Monocyte proliferation is regulated by MafB.
Fig.3 MafB restricts proliferation and mediates interstitial macrophage development.1	MafB expression is reduced in proliferating monocytes compared to cMo, while MafB expression is increased in IM. By constructing Mafb myeloid conditioned knockout mice, the researchers found that the myeloid restriction Mafb deficiency severely affected the ability of cMo to repopulate the IM subpopulation niche (Fig.3). These results suggest that monocyte proliferation requires a low level of MafB expression, and that subsequent increases in MafB expression limit proliferation and promote their differentiation into IM. In addition, the characteristics of CD206+ IM subsets are regulated by the transcription factor c-Maf.

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