IL17A and rheumatoid arthritis: Further, the mitochondrial transfer to the Th17 cells was impaired when co-culturing with human synovial MSCs (sMSCs) from patients with rheumatoid arthritis (RA) when compared with healthy BMSCs; in addition, this artificial MitoT also significantly reduced the IL-17 production in the Th17 cells, suggesting that a reduced mitochondrial transfer by the RA-sMSCs may be the main reason for the persistence of chronic inflammation in RA synovitis [38].