Myelin basic protein-(MBP)-specific T cells isolated from the peripheral lymphocytes of human individuals with MS and encephalitogenic T cells recovered from circulating 2 Clinical and Developmental Immunology autoreactive T cells of either immunized or naïve animals have shown that autoreactive T-cell lines that recognize the encephalitogenic part of MBP in vitro can be distinguished from an unprimed rat T-cell population. This confirms that autoreactive T cells play a central role in the pathology of MS [6] [7] [8] . EAE can also be induced by adoptively transferring an expanded population of myelin-reactive encephalitogenic CD4 + (T helper [Th] ) cells, which allows the further dissection of the immunopathogenic potency of different encephalitogenic CD4 + cell populations [9] . In the 1990s, Mosmann and Coffman postulated that Th cells can be classified into two distinct subsets, Th1 and Th2. Th1 cells produce large quantities of interferon γ (IFNγ), driven by interleukin 12 (IL12), which promotes cellular immunity directed against intracellular pathogens. Alternatively, Th2 cells, which secrete IL4, IL5, IL13, and IL25, are essential in the destruction of extracellular parasites and the mediation of humoral immunity [10, 11] . Selfreactive Th1 clones derived in vitro are capable of adoptively transferring EAE to naïve recipients [12] . Increased levels of Th1 cytokines are particularly evident during EAE/MS relapse, whereas increased Th2 cytokines are found during remission in MS patients when compared with control levels [13] . Clinical and hematological symptoms are exacerbated in relapsing/remitting MS patients following the administration of IFNγ, and this is also observed in other Th1type diseases, whereas it is less apparent in Th2 diseases [14, 15] . Th1 cells were earlier thought to be pathogenic T cells, whereas Th2 cells were thought to confer an antiinflammatory potential, constituting protective T cells in both MS and EAE [16] [17] [18] [19] .