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Fig. 8 | Journal of Neuroinflammation

Fig. 8

From: Estrogen-induced compensatory mechanisms protect IL-10-deficient mice from developing EAE

Fig. 8

Differential E2-mediated mechanisms of EAE protection in IL-10 KO vs WT mice. Treatment with E2 in WT mice results in the induction of IL-10-producing regulatory B cells (Bregs) that modulate T cells and macrophages through the secretion of IL-10 and the activation of PD-1 on T cells. This results in a decrease in pro-inflammatory Th1 and Th17 T cells and an increase in anti-inflammatory macrophages and microglia. Treatment with E2 increases PD-L1 and PD-L2 expression on macrophages. In the CNS, E2 decreases the frequency of CD11b+CD45hi cells and increases the frequency of CD11b+CD45lo microglial cells during EAE compared to sham-treated mice (a). Treatment with E2 in IL-10 KO mice results in an increase in the number of PD-L1 and PD-L2 positive macrophages compared to WT E2-treated mice. This results in the induction of activated CD4+CD25+ splenic T cells, an increase in Breg B10 and plasmablast Breg subsets expressing CD73, a marker for an IL-10 independent Breg immunoregulatory mechanism, an increase in CNS microglial cells, and a decrease in the frequency of Th1 and Th17 pro-inflammatory cells. This results in decreased levels of CD11b+CD45hi activated macrophages similar to WT E2-treated mice and a downregulation of pro-inflammatory mediators (b)

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