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Serum/glucocorticoid-inducible kinase 1 deficiency induces NLRP3 inflammasome activation and autoinflammation of macrophages in a murine endolymphatic hydrops model

GSDMD propagates oxidative damage to HCs via a self-reinforcing intercellular loop While oxidative stress initiates upstream of GSDMD signaling (Fig

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discovered that a novel in situ gel of TAC-loaded SLNs could suppress the release of inflammatory mediators from conjunctival mast cells, down-regulate IL-4 in serum, thereby inhibiting B cell antibody reactions from IgM to IgE, reducing IgE synthesis, up-regulating IFN- in serum, inhibiting Th2 cell proliferation and IL-4 function, suppressing the conversion of Th1 to Th2, and maintaining the dynamic balance of Th1 and Th2