Cross-reactivity between peptide mimics of the immunodominant myelin proteolipid protein epitope PLP139-151: comparison of peptide priming in CFA vs. viral delivery

Epidemiological evidence suggests that pathogens may trigger the development of autoimmune diseases such as multiple sclerosis (MS). Pathogens may trigger disease via molecular mimicry, wherein T cells generated against foreign epitopes are also cross-reactive with self-epitopes. Five pathogen-derived molecular mimics of PLP(139-151) (the immunodominant CD4(+) T cell myelin epitope in SJL mice) were previously identified. This study examines the degree of cross-reactivity between the different mimics, comparing mice primed with mimic peptide in CFA with mice infected with recombinant mimic-expressing viruses. The pattern of in vitro reactivity and ability to induce CNS disease differs between peptide priming and virus infection.