Regulatory role of natural killer (NK)-T cells for EAE

NK1.1+ natural killer (NK)-T cells reactive to CD1 appear to be involved in spontaneous autoimmune disease, but their role in induced autoimmune disease remains unclear. While we previously reported a regulatory role of NK cells in experimental autoimmune encephalomyelitis (EAE), we demonstrate here that NK-T cells would also play a pivotal role in the control of EAE. C57BL/6 (B6) mice selectively depleted for NK-T cells were generated by antibody-depended protocols or knocking out TCRJα281 gene. Regardless of the method for NK-T cell deletion, these NK-T depleted mice developed unusually early onset of EAE (5–8 days after challenge) after immunization with an encephalitogenic peptide myelin oligodendrocyte glycoprotein (MOG)35–55. The early EAE onset was associated with early induction of T helper cell type 1 (Th1) cells and marked elevation of Th1 cytokines in the serum. It was of note that, although the NK-T deficient mice spontaneously recovered from EAE, mice selectively depleted for NK cells developed a later onset of non-remitting EAE. These data establish differential roles played by NK-T and NK cells in the protection against EAE.