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Monocyte differentiation and macrophage priming are regulated differentially by pentraxins and their ligands
Darrell Pilling1, Elkin Galvis-Carvajal2, Tejas R Karhadkar2
1Department of Biology, Texas A&M University, 3474 TAMU, College Station, TX, 77843-3474, USA. dpilling@bio.tamu.edu.
Background:
Circulating bone marrow-derived monocytes can leave the blood, enter a tissue, and differentiate into M1 inflammatory, M2a remodeling/fibrotic, or M2c/Mreg resolving/immune-regulatory macrophages. Macrophages can also convert from one of the above types to another. Pentraxins are secreted proteins that bind to, and promote efficient clearance of, microbial pathogens and cellular debris during infection, inflammation, and tissue damage. The pentraxins C-reactive protein (CRP), serum amyloid P (SAP), and pentraxin-3 (PTX3) can also bind a variety of endogenous ligands. As monocytes and macrophages are exposed to differing concentrations of pentraxins and their ligands during infection, inflammation, and tissue damage, we assessed what effect pentraxins and their ligands have on these cells.
Results:
We found that many polarization markers do not discriminate between the effects of pentraxins and their ligands on macrophages. However, pentraxins, their ligands, and cytokines differentially regulate the expression of the hemoglobin-haptoglobin complex receptor CD163, the sialic acid-binding lectin CD169, and the macrophage mannose receptor CD206. CRP, a pentraxin generally thought of as being pro-inflammatory, increases the extracellular accumulation of the anti-inflammatory cytokine IL-10, and this effect is attenuated by GM-CSF, mannose-binding lectin, and factor H.
Conclusions:
These results suggest that the presence of pentraxins and their ligands regulate macrophage differentiation in the blood and tissues, and that CRP may be a potent inducer of the anti-inflammatory cytokine IL-10.
Insights
Pentraxins and their ligands influence how monocytes and macrophages differentiate and function. C-reactive protein (CRP) may significantly increase anti-inflammatory cytokine IL-10, impacting immune responses.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- Monocytes differentiate into macrophages (M1, M2a, M2c/Mreg) in tissues, with potential for interconversion.
- Pentraxins (CRP, SAP, PTX3) clear pathogens and debris, and bind endogenous ligands.
- Monocytes/macrophages encounter varying pentraxin/ligand levels during inflammation and tissue damage.
Purpose of the Study:
- To investigate the effects of pentraxins and their ligands on monocyte and macrophage differentiation and function.
- To identify specific markers regulated by pentraxins and their ligands in these cells.
Main Methods:
- Assessed the impact of pentraxins, ligands, and cytokines on monocyte/macrophage polarization markers.
- Quantified the expression of CD163, CD169, and CD206 under different treatment conditions.
Main Results:
- While many polarization markers were similar, pentraxins, ligands, and cytokines differentially regulated CD163, CD169, and CD206 expression.
- C-reactive protein (CRP) increased extracellular IL-10 accumulation, an effect modulated by GM-CSF, mannose-binding lectin, and factor H.
Conclusions:
- Pentraxins and their ligands modulate macrophage differentiation in blood and tissues.
- CRP may act as a significant inducer of the anti-inflammatory cytokine IL-10.
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