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The once widely accepted primary role for β-amyloid in sporadic AD (known as the amyloid cascade hypothesis) is currently criticised as not being the sole cause of AD, but nevertheless, amyloid accumulation is clearly a part of AD pathology and evokes multifaceted glial responses

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IL-6 and TGF-β signaling in naïve CD4+T cells promote expression of RORγt, which in turn drives the differentiation of Th17 cells secreting IL-17A, IL-17F, IL-22, and IL-23R, as seen in Supplementary Figure 2D ( Supplementary Data of Supplementary Materials