Interleukin-4 deficiency facilitates development of experimental myasthenia gravis and precludes its prevention by nasal administration of CD4(+) epitope sequences of the acetylcholine receptor

Immunization with acetylcholine receptor (AChR) causes experimental myasthe nia gravis (EMG). We investigated EMG in interleukin (IL)-4 knock out B6 (K O) mice, that lack Th2 cells. EMG was mon frequent in KO than in wild type B6 mice. KO and B6 mice developed similar amounts of anti-AChR antibodies. They were IgG2a and IgG2b in KO mice, IgG1 and IgG2b in B6 mice. CD4(+) cel ls from KO and B6 mice recognized the same AChR epitopes. Nasal administrat ion of synthetic AChR CD4(+) epitopes reduced antibody synthesis and preven ted EMG in B6, not in KO mice. Thus, Th2 cells may have protective function s in EMG. (C) 1999 Elsevier Science B.V. All rights reserved.