The immunomodulating neuropeptide alpha-melanocyte-stimulating hormone (α-MSH) suppresses LPS-stimulated TLR4 with IRAK-M in macrophages
Abstract
Since alpha-MSH suppresses endotoxin-induced inflammation by innate immunity, it is possible that alpha-MSH can suppress the interface between innate and adaptive immunity mediated by TLR4-stimulated macrophages. Endotoxin-stimulated macrophages treated with alpha-MSH are suppressed in nitric oxide and IL-12p70 production, and cannot enhance antigen-stimulated IFN-gamma production by Th1 cells. In macrophages treated with alpha-MSH, the inhibitory molecule IRAK-M is bound to IRAK-1, the proximal intracellular signal molecule of endotoxin-bound TLR4. These results further demonstrate the dynamic contribution of the nervous system, and the role of alpha-MSH in modulating the innate and adaptive immune interface in an inflammatory response.
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Cited By (10)
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- Endogenous Cortisol and TGF-β in Human Aqueous Humor Contribute to Ocular Immune Privilege by Regulating Dendritic Cell FunctionThe Journal of Immunology · 2011
- The Role of Retinal Pigment Epithelial Cells in Regulation of Macrophages/Microglial Cells in Retinal ImmunobiologyFrontiers in Immunology · 2021
- Ocular immune privilege and retinal pigment epithelial cellsJournal of Leukocyte Biology · 2023
- Anti-inflammatory Properties of the Alpha-Melanocyte-Stimulating Hormone in Models of Granulomatous InflammationLung · 2022
- The melanocortin system in control of inflammation
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