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The Treg/Th17 cell axis refers to the dynamic balance between regulatory T cells, which suppress immune activation and promote tolerance, and T helper 17 cells, which drive inflammation and support pathogen clearance[1][5][2][3][4][6]. Both cell types originate from naïve CD4+ T cells, whose differentiation is influenced by cytokine milieu (TGF-β, IL-6, IL-21, IL-23) and metabolic pathways (glycolysis vs. fatty acid oxidation)[1][2][5][4][6]. Their balance is tightly regulated; disruption favors either excessive inflammation (Th17 dominance, as in autoimmunity) or immune suppression (Treg dominance, as in cancer)[1][5][2][3]. Therapeutics target cytokine pathways, metabolism, and epigenetic regulation to restore healthy immune balance, making the axis a key target in immunology and drug development.
Promoting Treg differentiation by blocking proinflammatory cytokines (e.g., anti-IL-6, retinoic acid); Inhibiting Th17 differentiation via mTOR inhibition/glucose deprivation; Targeting IL-17/IL-23/IL-6 signaling; Epigenetic or metabolic reprogramming of T cells
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