TLR4 and myeloid sarcoma: Indeed, genetic knockout studies using experimental autoimmune encephalomyelitis (EAE) indicate that TLR4 [9], TRIF [10], and IFN-β [11] deficiency exacerbate EAE, while knockout of MyD88 [9,12,13] and IRF3 [14] is protective in EAE, indicating the complex role of TLR pathways in inflammatory changes associated with mouse models of MS.