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While the reduction in disease progression was correlated to the modulation of macrophage activity, in contrast to the administration of the ES products, FhHDM-1-mediated protection was associated with the reduced ability of macrophages to respond to pro-inflammatory ligands, suggesting the regulation of an M1-like phenotype, and indicating multiple mechanisms mediating an overall switch from a predominance of pro-inflammatory to anti-inflammatory macrophages (104)

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