Fig. 4: O4+ cells intrinsically synthesize molecules of the Immune/inflammatory pathways in response to neuroinflammation (See Fig. S2).

A Validation of the induction of gene expression for members of the GO-term “immune system and inflammatory response pathways” by neuroinflammation, in O4+ cells at P5, using RT-qPCR. Number of independent experiments: n = 8 for all genes, except for Cxcl9, Cxcl10, and Il1r1 (n = 7). *p < 0.05; **p < 0.01; ***p < 0.001. Gray bars: ligands; black bars: receptors. B In vitro cultured OPCs intrinsically secrete mediators of the immune and inflammatory pathways in response to inflammatory stimulus. (Upper panel) Experimental design for ex vivo OPC culture, inflammatory exposure (IL1B), and differentiation (see Material and Methods). (Lower panels) Protein detection and quantification (pG/mL) of the expression of interleukins (IL1B, IL6), cytokine C-C Motif Chemokine Ligand 2, 4, and 5 (CCL2, CCL3, CCL4, and CCL5) and chemokine C-X-C Motif Chemokine Ligand 2 (CXCL2) by Luminex. CTR, PBS exposure; IL1B, IL1B exposure. The dotted line represents the limit of detection for individual proteins in the assay. The numbers of independent experiments performed for each plot are indicated on each plot. *p < 0.05; **p < 0.01; ***p < 0.001. C Upregulation of genes of the immune/inflammatory pathways, in the oligodendroglial cell line, Oli-neu, and downregulation of the myelination program, upon inflammatory stimulus. Treatment of the Oli-neu cell line by TFN-alpha reproduces the disturbances in gene expression that we observed in isolated O4+ cells upon in vivo neuroinflammation. (Upper panel) Experimental design. (Lower panels) RT-qPCR analyses for myelinations markers and proinflammatory mediator genes Cnp and Mbp, and Ccl2 and Cxcl10, respectively. n = 6 independent experiments. Nonparametric t-tests; **p < 0.01. Time 0: undifferentiated cells.