In an experimental autoimmune encephalomyelitis (EAE) model, overexpression TRIM37 significantly suppressed neuroinflammation mediated by microglia, reduced the expression of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), and alleviated demyelination lesions (as evidenced by reduced myelin damage shown by Luxol fast blue (LFB) staining, P < 0.001), while simultaneously increasing MBP expression levels (P < 0.001). Here, IL1B is linked to experimental autoimmune encephalomyelitis.