Rethinking EAE pathogenesis

Th1 cells have long been thought to mediate the pathogenesis of experimental autoimmune encephalitis (EAE), a mouse model for multiple sclerosis. But Langrish et al. now identify a new subset of T cells as the driving force behind brain inflammation in EAE (page 233).

Previous thinking on EAE culprits has focused on Th1 CD4⁺ T cells and their distinctive product IFN-γ, both of which are found at EAE inflammation sites. But the details were confused by the biology of p40—a subunit shared by both IL-12 (an inducer of Th1 cells) and IL-23. This group showed recently that EAE is suppressed after p40 inactivation because of the loss of IL-23 not IL-12.

The authors now explain the pathogenic effect of IL-23 by showing that this cytokine...