To date, the therapeutic effect of IFN-â in MS has mainly been attributed to direct anti-inflammatory effects, either systemically through alteration of immune cell states or locally at the BBB through down-regulation of several molecules, and previous reports have demonstrated reduced CXCR3+ Th1 activities or IL-10 (Th2 cytokine) induction by IFN-â treatment in MS patients [26]. Here, CXCR3 is linked to myeloid sarcoma.