Figure 1.

An-IL-17-mediated hypothesis of depressive disorder in an experimental model. In a young adult depression mouse model exposed to cumulative mild stress (CPMS) characterized by microglial activation, IL-17 in brain and blood, as well Th-17 cells are elevated. A hypothesis based on the assumption that microglia activation is pivotal for the increase of pro-inflammatory cytokines such as IL-16 and TGF-b, which polarize CD4+ T cells towards Th-17 is formulated. Experimental data suggest that anti-IL-17 mAb treatment, diminishes IL-17 induction and Th-17 differentiation and ameliorates anxiety and depression-like behaviors (61) (prepared with BioRender).