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*
Microbiology and Tumor Biology Center, Karolinska Institutet, Stockholm, Sweden;
Division of Neurology, Huddinge University Hospital, Karolinska Institutet, Stockholm, Sweden; and
Section of Cytokine Biology, Biomedical Primate Research Center, Rijswijk, The Netherlands
Autoantigen administration via nasal mucosal tissue can induce
systemic tolerance more effectively than oral administration in a
number of experimental autoimmune diseases, including Ab-mediated
experimental autoimmune myasthenia gravis, a murine model of myasthenia
gravis. The mechanisms underlying nasal tolerance induction are not
clear. In this study, we show that nasal administration of
acetylcholine receptor (AChR) in C57BL/6 mice, before immunizations
with AChR in adjuvant, results in delayed onset and reduced muscle
weakness compared with control mice. The delayed onset and reduced
muscle weakness were associated with decreased AChR-specific lymphocyte
proliferation and decreased levels of anti-AChR Abs of the IgG2a
and IgG2b isotypes in serum. The clinical and immunological changes in
the AChR-pretreated C57BL/6 wild-type (wt) mice were comparable with
those observed in AChR-pretreated CD8-/- mice, indicating
that CD8+ T cells were not required for the generation of
nasal tolerance. AChR-pretreated wt and CD8-/- mice
showed augmented TGF-ß and reduced IFN-
responses, whereas levels
of IL-4 were unaltered. Splenocytes from AChR-pretreated wt and
CD8-/- mice, but not from CD4-/- mice,
suppressed AChR-specific lymphocyte proliferation. This suppression
could be blocked by Abs against TGF-ß. Thus, our results demonstrate
that the suppression induced in the present model is independent of
CD8+ T cells and suggest the involvement of Ag-specific
CD4+ Th3 cells producing TGF-ß.
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