ENHANCEMENT OF EAE AND INDUCTION OF AUTOANTIBODIES TO T-CELL EPITOPESIN MICE INFECTED WITH A RECOMBINANT VACCINIA VIRUS ENCODING MYELIN PROTEOLIPID PROTEIN

SJL/J mice were infected with a recombinant vaccinia virus encoding my elin proteolipid protein (PLP) (VVplp). Antibody responses to whole PL P and to encephalitogenic peptides, p139-151, p178-191 or p104-117 wer e measured after vaccination and following challenge with these three PLP peptides. Competitive ELISAs showed that antibodies to p139-151 an d p178-191 represented the majority of antibodies in the anti-PLP anti body response following VVplp vaccination, since the antibodies to int act PLP could be inhibited 56, 35 and 1%, respectively, by p139-151, p 178-191 and p104-117. After peptide challenge, epitope specific anti-p eptide antibodies were enhanced. These anti-peptide antibodies also re acted with the intact PLP molecule. Interestingly, the mean titer of a nti-p139-151 antibody in p139-151 challenged mice was significantly hi gher than that observed for anti-p178-191 in p178-191 and for anti-p10 1-117 in p104-117 challenged mice. Following peptide challenge, the an ti-PLP IgG response shifted from an IgG1 to an IgG2a and 2b phenotype. In these mice, both the clinical disease and histological pattern of experimental allergic encephalomyelitis (EAE) were enhanced. The enhan cement was most pronounced in the pathologic scores in the p139-151 ch allenged group followed by p104-117 challenged mice. Thus, humoral imm une responses to PLP encephalitogenic peptides can be generated with v irus encoding a self central nervous system (CNS) protein.