Here, we demonstrate that hiOL from RRMS patients and controls do not differ in their functionality or proteome; however, inflammatory mediators and especially IFNγ, released by T cells, inhibit oligodendroglial differentiation which cannot be restored by the application of oligodendroglial differentiation promoting drugs but can partly be enhanced by imunomodulatory treatment of PBMCs suggesting that the inflammatory environment in MS lesions is a major contributor to impaired remyelination in MS. Here, IFNG is linked to relapsing-remitting multiple sclerosis.