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Given the crucial role of Th17 cell-mediated immune inflammation in the progression of psoriasis, we speculate that GLUT3 may participate in the pathogenesis of psoriasis by regulating the aerobic glycolysis of Th17 cells, and further experiments are needed to verify this possibility

Thus, not only can an infectious agent better survive in a poorly directed immune response, but if autoantibodies are directed against critical molecules (ACTH), the infection can thrive in a host with a weaker immune system (42)

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