Fig. 7.

Proposed model for IL-10 regulation of neuroinflammation and tau pathology. A In non-transgenic (Non-Tg) mice, we observed an increase in proinflammatory cytokines, including IL-6, TNFα, and IL-1β, with a concomitant increase in anti-inflammatory cytokine, IL-10. IL-10 provides negative feedback to dampen cytokine production, microglial activation, and p38 MAPK activation resulting in only low levels of tau phosphorylation. B In IL-10-deficient mice (Il10^−/−), the absence of IL-10 leads to enhanced cytokine production, especially for IL-6 and TNF, microglia are more active and more amoeboid, and p38 MAPK levels are also enhanced. Tau phosphorylation is exacerbated in neuronal bodies of the Il10^−/− brains. Created with BioRender.com