International Immunology, Vol 10, 1359-1365, Copyright © 1998 by Oxford University Press
H Li, FD Shi, B He, M Bakheit, B Wahren, A Berglof, K Sandstedt and H Link
Experimental autoimmune myasthenia gravis (EAMG) is an animal model for
human myasthenia gravis (MG). Autoantibody-induced functional loss of
nicotinic acetylcholine receptor (AChR) at the postsynaptic membrane is an
important pathogenic feature of both MG and EAMG. To evaluate the extent at
which the humoral immune response against AChR operates in the pathogenesis
of EAMG, we immunized B cell knockout (muMT) and wild- type C57BL/6 mice
with AChR and complete Freund's adjuvant. The ability of AChR-primed lymph
node cells to proliferate and secrete IFN-gamma in response to AChR and its
dominant peptide alpha146-162 were intact in muMT mice as in wild-type
mice. Similar amounts of mRNA for IFN-gamma, IL-4 and IL-10 in
AChR-reactive lymph node cells were detected in muMT and wild-type mice.
However, muMT mice had no detectable anti-AChR antibodies and remained
completely free from clinical EAMG. We conclude that B cells are critically
required for the genesis of clinical EAMG, but not for AChR-specific T cell
priming.
ARTICLES
Experimental autoimmune myasthenia gravis induction in B cell-deficient mice
Division of Neurology, Karolinska Institute, Stockholm, Sweden.
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