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Receptor Deficiency Are Less Susceptible to Experimental Autoimmune Myasthenia Gravis1
*
Division of Neurology, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden;
Biomedical Primate Research Center, Rijswijk, The Netherlands; and
Microbiology and Tumor Biology Center, Karolinska Institute, Stockholm, Sweden
IFN-
can either adversely or beneficially affect certain
experimental autoimmune diseases. To study the role of IFN- in the
autoantibody-mediated experimental autoimmune myasthenia gravis (EAMG),
an animal model of myasthenia gravis in humans, IFN-R-deficient
(IFN-R-/-) mutant C57BL/6 mice and congenic wild-type
mice were immunized with Torpedo acetylcholine receptor
(AChR) plus CFA. IFN-R-/- mice exhibited significantly
lower incidence and severity of muscle weakness, lower anti-AChR
IgG Ab levels, and lower Ab affinity to AChR compared with wild-type
mice. Passive transfer of serum from IFN-R-/- mice
induced less muscular weakness compared with serum from wild-type mice.
In contrast, numbers of lymph node cells secreting IFN- and of those
expressing IFN- mRNA were strongly augmented in the
IFN-R-/- mice, reflecting a failure of negative
feedback circuits. Cytokine studies by in situ hybridization revealed
lower levels of lymphoid cells expressing AChR-reactive IL-1ß and
TNF-
mRNA in AChR + CFA-immunized IFN-R-/- mice
compared with wild-type mice. No differences were found for
AChR-reactive cells expressing IL-4, IL-10, or TGF-ß mRNA. These
results indicate that IFN- promotes systemic humoral responses in
EAMG by up-regulating the production and the affinity of anti-AChR
autoantibodies, thereby contributing to susceptibility to EAMG in
C57BL/6-type mice.
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