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IL-23 is indispensable in the survival, amplification and pathogenicity of Th17 cells in the late stage of Th17 differentiation[22].On the contrary, induced Treg (iTreg) cells is driven by high concentrations of TGF-, T-cell receptor (TCR) signaling and IL-2

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Autophagy enhances intestinal epithelial tight junction barrier function by targeting claudin-2 protein degradation

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Animal studies have shown that it accelerates the healing of a wide variety of wounds, including muscles, tendons and damaged ligaments