CCR7 and lysosomal storage disease: It also enhanced the inhibitory expression of co-stimulatory molecules Cd80 and Cd83; adhesion molecule Icam1; cytokines TNF-α, IL-1β, and IL-6; chemokine receptor Ccr7; and antigen-presenting molecules MHC II and MHC I. By contrast, TFEB or TFE3 overexpression partially alleviated the As-induced inhibitory effects of DC lysosomal disorder, autophagic flux blockade, and immune dysfunction.