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Autoimmunity

Interfering with brain inflammation

Nature Reviews Immunology volume 12, page 77 (2012)Cite this article

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The authors looked at the role of the RNA helicases RIG-I and MDA5 — stimulation of which is known to induce type I IFN production — in the context of experimental autoimmune encephalomyelitis (EAE) in mice. Similarly to human multiple sclerosis, EAE is thought to be mediated by T helper 1 (TH1) and TH17 cells. In mice lacking the RIG-I and MDA5 adaptor protein MAVS (also known as IPS1, VISA and CARDIF) that were immunized with a myelin-associated antigen, the peak clinical EAE disease score was markedly increased compared with that of wild-type mice. This correlated with increased numbers of macrophages and T cells in the CNS and increased demyelination. The encephalitogenic T cell response in Mavs−/− mice was shifted further towards TH1 and TH17 cell responses compared with that of wild-type mice, as shown by the increased expression of cytokines and transcription factors associated with these subsets.

These results indicate that the RNA helicases might have a protective role in EAE, and this was confirmed by the administration of ligands for RIG-I and MDA5 to wild-type mice at the peak of disease. Treated mice had markedly decreased disease severity and greatly increased serum levels of IFNβ. The transcripts of TH1 and TH17 cell-associated factors were decreased in number in the CNS of mice treated with RIG-I and MDA5 ligands.

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ORIGINAL RESEARCH PAPER

  1. Dann, A. et al. Cytosolic RIG-I-like helicases act as negative regulators of sterile inflammation in the CNS. Nature Neurosci. 4 Dec 2011 (doi:10.1038/nn.2964)

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  1. Kirsty Minton
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Minton, K. Interfering with brain inflammation. Nat Rev Immunol 12, 77 (2012). https://doi.org/10.1038/nri3154

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