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Fig. 2 | Journal of Neuroinflammation

Fig. 2

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

Fig. 2

E2-treated IL-10 KO mice increase PD-1 ligand expression on CD11b+ cells in the spleen and LN. E2 treatment resulted in a significant increase in the number of PD-L1-expressing CD11b+ cells in the spleen in both WT and IL-10 KO mice compared to sham (p < 0.001) and significantly increased the number of PD-L1-expressing CD11b+ cells in IL-10 KO mice (n = 8 for both groups) compared to WT sham (n = 6) and E2-treated (n = 8) groups, (p < 0.05; a). PD-L1 frequency was also significantly increased in E2-treated groups compared to sham-treated groups for WT (n = 6 and n = 8, respectively) and IL-10 KO mice (n = 8 for both groups) in the inguinal lymph nodes (p < 0.05; b). The number of PD-L2-expressing CD11b+ cells was significantly increased in the E2-treated groups compared to the sham-treated groups for both WT (n = 6 and n = 8, respectively) and IL-10 KO (n = 8 for both groups) in the spleen (p < 0.05). PD-L2-expressing CD11b+ cells were also significantly increased in the IL-10 KO mice compared to WT mice for both treatment groups (p < 0.05; c). In the inguinal lymph nodes, the frequencies of PD-L2 on CD11b+ cells were significantly increased in the IL-10 KO E2-treated mice (n = 8) compared to the WT-treated mice (n = 8; p < 0.05; d). Additionally, IL-10 KO mice (n = 3) treated with E2 have no significant differences in gene expression of PD-L1 in the spinal cord compared to E2-treated WT mice (n = 3; e). IL-10 KO mice treated with E2 have significantly higher gene expression of PD-L2 (p < 0.05) in the spinal cord compared to WT mice treated with E2 (f). Data are represented as mean ± SEM

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