The B cell repertoire in experimental allergic neuritis involves multiple myelin proteins and GM1

Experimental allergic neuritis (EAN) is a T cell mediated disease associated with inflammation and demyelination of peripheral nerves. EAN is an experimental model of Guillain-Barré syndrome. The peripheral nerve myelin components P2 and P0 represent major neuritogens, but the diversity and quantity of B cell responses in EAN are unknown. Lewis rats were immunized with bovine peripheral nerve myelin (BPM), and levels of B cells secreting IgM and IgG antibodies to BPM, P2 and P0, the glycolipid GM1 and five peptides of myelin-associated glycoprotein (MAG) were determined. Already on day 7 post-immunization (p.i.), i.e. before the onset of clinical EAN, lymph nodes contained elevated levels of cells secreting IgM antibodies of all specificities examined. Maximum numbers of IgG antibodies secreting cells were generally reached at the height of clinical disease. The numbers of cells secreting IgG antibodies to BPM, P2, P0, GM1 and MAG peptides were also elevated before disease onset, but they were mostly higher than those of IgM antibodies and they reached their maximum only after recovery. The results imply that EAN is associated with strong B cell responses to all myelin antigens under study without restriction to any immunodominant myelin component or MAG peptides.