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In arthritis models with diminished endogenous MaR1 expression, exogenous MaR1 administration prevents macrophage recruitment to the dorsal root ganglia and reverses pain hypersensitivity [259]

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M1 macrophages play a key role in the initial stages of the inflammatory response by releasing considerable amounts of inflammatory agents such as tumor necrosis factor (TNF-), IL-6 and IL-12, which contribute to aggravating inflammation

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