A similar effect was observed for cells from donors not affected with autoimmune disease, where exosomes from proinflammatory astrocytes increased CCL2 production, and the amount of CCL2 was significantly higher in T-cells culture exposed to exosomes from proinflammatory astrocytes, as compared to exosomes from TGF-β-primed astrocytes. This evidence concerns the gene TGFB1 and autoimmune disease.