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Although the mechanism that leads to the depletion of Th17 cells remains largely unknown, some of the proposed mechanisms include (i) a lack of HIV-inhibitory RNases in human Th17 cells leading to early, sustained depletion [59], (ii) decreased levels of IL-21-producing cells responsible for maintaining Th17 cells [60], and (iii) a depletion of CD103+ dendritic cells which promote Th17 differentiation [61]

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This leads to an accumulation of globotriasylceramide (Gb3) in lysosomes, resulting in various vascular complications in the kidneys, heart, skin, and brain and a reduced life expectancy

48 MiR-128-3p simultaneously inhibits the expression of AXIN1, SFRP2, and WIF1 to enhance the activity of the Wnt/-catenin signalling pathway, thus promoting non-small cell lung cancer (NSCLC) metastasis