Multiple sclerosis (MS) is a disease presumably associated with chronic immune stimulation promoted by either pathogens or autoimmune processes. It has been hypothesized that MS could be the result of previous viral infections rendering a permanent immune stimulation that could be triggered by molecular similarities, or by modulating the antigens expression of major histocompatibility complex (MHC) on target cells, which in turn act as super antigens. During immune stimulation occurs the recruitment of immunological cells, resulting in local tissue damage and leading to the release of damage- associated molecular patterns (DAMPs), which also act as inflammation inducers. Recently, it has been proposed that the association between pathogen-associated molecular patterns (PAMPs) with DAMPs constitutes an additional level of immune regulation. The properties of DAMPs to act as carriers of PAMPs and their role as enhancers or inhibitors of PAMPs could play a role during inflammatory responses triggered by infections. Here, we focused this review in outcomes which support the hypothesis that particular PAMP-DAMPs interactions could regulated the relapse and progressive disability observed in multiple sclerosis.