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Reprogramming suppressive nutrient and lipid milieus to support dendritic cell priming and T cell activation A second group of therapies more directly targets the metabolic crosstalk between tumour cells, myeloid cells, DCs and T cells

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Microglial activation can result in pro-inflammatory conditions, characterized by the secretion of pathological factors (such as IL-1β, TNF-α, IL-6, NO, and proteases), or in neuroprotective states, influenced by signals like IL-4, IL-10, IL-13, and transforming growth factor-β (TGF-β) [50]

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