In this model, administration of antiserum to IFN-beta or poly(I:C), a TLR3 agonist mimicking a dsRNA viral infection, leads to more severe demyelinating disease by promoting ‘virus-like’ activity, specifically the recruitment and activation of ‘bystander’ immune cells within the tissue such as microglia and astrocytes [43]. Here, TLR3 is linked to demyelinating disease.