Endogenous, or therapeutically induced, type I interferon responses differentially modulate Th1/Th17-mediated autoimmunity in the CNS

20.03.2012

Kalinke U, Prinz M.

Immunol Cell Biol. 2012;90(5):505-9

Immunol Cell Biol      online article

Various different viruses trigger pattern recognition receptor systems such as Toll-like receptors (TLR) or cytosolic RIG-I like helicases (RLH) and thus induce early type I interferon (IFN-I) responses. Interestingly, the same innate immune mechanisms that are relevant for early pathogen defense play a role in ameliorating experimental autoimmune encephalomyelitis (EAE), a rodent model of human multiple sclerosis. We and others found that mice devoid of the IFN-I receptor showed significantly enhanced autoimmune disease of the CNS. These experiments are consistent with the hypothesis that spatiotemporal conditions of, and cell types involved in, disease ameliorating IFN-I responses differ
significantly, depending on whether they were endogenously induced in context of EAE pathogenesis within the CNS or upon therapeutic RLH triggering in the periphery. It is attractive to speculate that RLH triggering represents a new strategy to treat multiple sclerosis.