IL-12Rβ2 has a protective role in relapsing-remitting experimental autoimmune encephalomyelitis

- IL-12Rβ2−/− EAE mice showed more severe symptoms and had stronger relapses.
- More infiltrating MNCs and Th17 cells were found in the CNS of IL-12Rβ2−/− EAE mice.
- Splenocytes of IL-12Rβ2−/− EAE mice had higher proliferative capacity.
- Splenocytes of IL-12Rβ2−/− EAE mice produced less IFN-γ.
- We suggest a protective role of IL-12Rβ2 signaling in relapsing-remitting-EAE.

IL-12Rβ2 is a common receptor subunit of heterodimeric receptors for IL-12 and IL-35, two cytokines that are implicated in immunopathogenesis of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. We evaluated the role of IL-12Rβ2 in relapsing-remitting EAE (RR-EAE). IL-12Rβ2-deficient SJL/J mice developed markedly more severe clinical EAE, and had greater mortality and more severe relapses compared with wild-type controls. IL-12Rβ2-deficient EAE mice also had more infiltrating mononuclear cells in the CNS, as well as higher T cell proliferative capacity and decreased IFN-γ production at the periphery. These findings demonstrate a protective role of IL-12Rβ2 in RR-EAE.

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