Myasthenia gravis is one of the typical organ specific autoimmune disease a
nd the CD5(+) B-lymphocytes are known to be associated with the secretion o
f autoimmune antibodies. The authors performed the study to establish an an
imal model of experimental autoimmune myasthenia gravis (EAMG) by immunizin
g the nicotinic acetylcholine receptor (AChR) and to understand CD5(+) B-ly
mphocyte changes in peripheral blood of EAMGs, Lewis rats weighing 150-200
g were injected subcutaneously three times with 50 mu g AChR purified from
the electric organ of Torpedo marmorata and Freund's adjuvant. The EAMG ind
uction was assessed by evaluating clinical manifestations, The CD5(+) B-lym
phocyte was double stained using monoclonal PE conjugated anti-CD5(+) and F
ITC conjugated anti-rat CD45R antibodies and calculated using a fluorescenc
e-activated cell sorter (FACS), In three out of ten Lewis rats injected wit
h purified AChR, the EAMG models were established. The animals showed defin
ite clinical weakness responded to neostigmine; they had difficulty in clim
bing the slope, or easily fell down from a vertical cage, The range of CD5(
+) B-lymphocytes of peripheral blood in the EAMG models was 10.2%-17.5%, wh
ich was higher than in controls. In conclusion, the EAMG models were succes
sfully established and the CD5(+) B-lymphocyte expression in peripheral blo
od increased in EAMGs, This provided indirect evidence of the autoimmune pa
thomechanism of human myasthenia gravis.