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Intravenous injection of lipid-free apolipoprotein A-I dampens inflammation by reprogramming macrophage function
Injecting lipid-free apolipoprotein A-I reduces inflammation by changing immune cell behavior
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Abstract
Apolipoprotein A-I (apoA-I) shows specific uptake by macrophages and may influence immune responses in inflammatory conditions.
- Intravital imaging in mice demonstrates that lipid-free apoA-I is specifically taken up by dermal perivascular macrophages.
- Supraphysiological doses of apoA-I are associated with alterations in key cellular pathways, including mTORC1 and IRF8, in macrophages.
- ApoA-I pretreatment is linked to a reduction in inflammatory responses and immune cell trafficking during LPS-induced skin inflammation.
- In a mouse model of rheumatoid arthritis, apoA-I appears to inhibit joint inflammation.
- ApoA-I may serve as an integrator of vascular-immune interactions by modulating macrophage function near blood vessels.
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