A recent report has suggested that IFN-β attenuates the course and severity of MS by regulating inflammasome activation and subsequent IL-1 production [106]; they found that type 1 interferon potently repressed the activity of the NLRP1 and NLRP3 inflammasomes, thereby suppressing caspase-1 dependent IL-1β secretion in mice and MS patients; the inhibitory effect of IFN-β is mediated by innate immune cells, such as macrophages and DCs, which inhibit T helper 17 (TH17) responses through interleukin-27 (IL-27) [107, 108] (Figure 2). This evidence concerns the gene IL1B and myeloid sarcoma.