Figure 6.
Exosomal miR-142 Controls CD4+ T Cell Inflammatory Responses by Targeting SOCS1
(A) Screening scheme for target genes that might contribute to T cell inflammation mediated by miR-142. (B) Relative mRNA expression of the target gene SOCS1 in CD4+ T cells treated with miR-142 mimic NC, miR-142 mimic, inhibitor NC, or miR-142 inhibitor. (C) Representative blots showing protein expression of the target SOCS1 in CD4+ T cells treated with miR-142 mimic NC, miR-142 mimic, inhibitor NC, or miR-142 inhibitor. (D) Relative mRNA expression of SOCS1 in CD4+ T cells after exosome incubation. (E) The matched base pairs in the binding region of miR-142 and the reporter plasmids containing the wild- or mutant-type SOCS1 are shown. (F) Relative luciferase reporter activity of vectors carrying the luciferase gene and a fragment of SOCS1 3′UTR with wild- or mutant-type miR-142 binding sites after cotransfection with miR-142 mimic NC, miR-142 mimic, inhibitor NC, or miR-142 inhibitor. (G-I) Percentages of Th1 (G), Th17 (H), and Treg (I) proportions were calculated in CD4+ T cells transfected with SOCS1 and incubated with exosomes by flow cytometry. (J–L) Levels of the cytokines IFN-γ (J), IL-17A (K), and IL-10 (L) were measured in CD4+ T cells transfected with SOCS1 and incubated with exosomes. Data are presented as the means ± SEM (n = 6); ∗p < 0.05.