CpG Type A Induction of an Early Protective Environment in Experimental Multiple Sclerosis

What is it about?

Our data thus identify a link between TLR9 activation by specific ligands and the induction of tolerance via innate immunity mechanisms.

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Why is it important?

We found that treatment with CpG type A ODN (CpG-A), known to induce high amounts of IFN- in pDCs, significantly reduced disease severity in EAE, relative to controls ( versus , resp.; ). Treatment also delayed onset of neurological deficits and reduced spinal cord demyelination, while increasing the percentage of splenic regulatory (Foxp3+ CD4+) T cells. CpG-A likewise reduced the levels of IL-17 and IFN-γ in the CNS. Mechanistic insight into those events showed that CpG-A promoted a regulatory phenotype in pDCs. Moreover, adoptive transfer of pDCs isolated from CpG-A-treated mice inhibited CNS inflammation and induced disease remission in acute-phase EAE.