Recently, a novel effector T-cell subset, Th9 cells, has been identified, and the ability of this T-cell subset to induce EAE is currently being investigated. Jäger et al. generated Mog-specific Th17, Th1, Th2, and Th9 cells in vitro to directly characterize their encephalitogenic potency after their adoptive transfer. They found that Mog-specific Th1, Th17, and Th9 cells, but not Th2 cells, induce EAE. Interestingly, each T-cell subset induced disease in a distinct pathological manner, suggesting that the different effector Th subsets that induce EAE do so differently and implying that the pathological heterogeneity in MS lesions might be partly attributable to various characteristics of myelinreactive effector T cells [92] . The authors also suggested that MS might be a disease caused by multiple distinct myelinreactive effector cells. The disease induced by Th17 cells in some animals exhibited symptoms atypical of EAE, including ataxia, severe imbalance, and weight loss associated with high mortality. Some animals had a mixture of atypical and typical EAE symptoms. When cells were recovered from the CNS, it appeared that the transferred Th9 cells produced IFNγ. The identities of the other cell populations did not seem to drift after their in vivo transfer [93] .