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Departments of Biochemistry, Molecular Biology and Biophysics, and Pharmacology, University of Minnesota, Minneapolis, MN 55455
Myasthenia gravis (MG) is a T cell-dependent, Ab-mediated
autoimmune disease. Ab against muscle acetylcholine receptor (AChR)
cause the muscular weakness that characterizes MG and its animal model,
experimental MG (EMG). EMG is induced in C57BL6 (B6) mice by three
injections of Torpedo AChR (TAChR) in adjuvant. B6 mice
develop anti-TAChR Ab that cross-react with mouse muscle AChR, but
their CD4+ T cells do not cross-react with mouse AChR
sequences. Moreover, murine EMG is not self-maintaining as is human MG,
and it has limited duration. Several studies suggest that IL-4 has a
protecting function in EMG. Here we show that B6 mice genetically
deficient in IL-4 (IL-4-/-) develop long-lasting muscle
weakness after a single immunization with TAChR. They develop chronic
self-reactive Ab, and their CD4+ T cells respond not only
to the TAChR and TAChR 
subunit peptides, but also to several mouse
AChR subunit peptides. These results suggest that in B6 mice,
regulatory mechanisms that involve IL-4 contribute to preventing the
development of a chronic Ab-mediated autoimmune response to the
AChR.
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