The daily challenge of dodging pathogenic infections is carried out by the two arms of our immune system: the innate and the adaptive immune system. Innate immune cells, like neutrophils and dendritic cells (DCs), form the first line of defense against invading pathogens. Neutrophils are the most abundant cell type of the innate immune system and they can directly kill invading pathogens, a non-specific and rapid response. DCs are important orchestrators of adaptive immune responses, by adequately activating them, while maintaining immune tolerance against autoantigens and harmless antigens, e.g., dietary nutrients. The induction of peripheral tolerance by DCs and how neutrophils are able to shape DC-driven T cell development is explained. The current knowledge on the effects of tolerogenic adjuvants vitamin D3 (VD3), vitamin A-derivative retinoic acid (RA) and corticosteroid dexamethasone (DEX) on both DCs and neutrophils is described. In this thesis, we investigated the effects of these adjuvants on neutrophils and on DC-driven T cell development. We demonstrate that tolerogenic adjuvants VD3 and RA that could be used in DC-targeting therapies inhibit T helper 17 cell development, while they can also directly affect neutrophils. While DEX shows inhibitory effects on the function of stimulated neutrophils, RA increases neutrophil function. Therefore, we envision that combining a tolerogenic adjuvant-loaded DC-targeting nanoparticle with DEX treatment could be a valuable treatment strategy for patients with chronic inflammatory diseases. This treatment would promote a tolerogenic adaptive immune response while reducing the harmful effects of neutrophils as seen in some autoimmune diseases, including rheumatoid arthritis.