The mechanisms underlying spontaneous remission of autoimmune diseases are presently unknown, though regulatory T cells are believed to play a major role in this process. We tested the hypothesis that Th2 and/or other T cell regulatory cytokines cause the spontaneous remission of experimental allergic encephalomyelitis (EAE), a model of Th1‐mediated autoimmunity. We analyzed the cytokine profile of lymph node and central nervous system‐infiltrating cells in individual SJL mice at different stages of proteolipid protein (PLP) 139 – 151 peptide‐induced EAE. We found that IFN‐γ slowly fades away after clinical recovery, whereas IL‐4, IL‐10 and transforming growth factor‐β remain low or undetectable. Our peptide‐results therefore suggest that regulatory T cells producing anti‐inflammatory cytokines are not involved in spontaneous remission of EAE and challenge the view that the Th1/Th2 balance has a key role in EAE regulation.