Nasal administration of μg doses of acetylcholine receptor (AChR) is effective in preventing the development of B cell‐mediated EAMG in the Lewis rat, a model for human MG. In order to investigate whether nasal administration of AChR modulates ongoing EAMG, Lewis rats were treated nasally with AChR 2 weeks after immunization with AChR and Freund's complete adjuvant. Ten‐fold higher amounts of AChR given nasally (600 μg/rat) were required to ameliorate the manifestations of EAMG compared with the amounts necessary for prevention of EAMG. In lymph node cells from rats receiving 600 μg/rat of AChR, AChR‐induced proliferation and interferon‐gamma (IFN‐γ) secretion were reduced compared with control EAMG rats receiving PBS only. The anti‐AChR antibodies in rats treated nasally with 600 μg/rat of AChR had lower affinity, reduced proportion of IgG2b and reduced capacity to induce AChR degradation. Numbers of AChR‐reactive IFN‐γ and tumour necrosis factor‐alpha (TNF‐α) mRNA‐expressing lymph node cells from rats treated nasally with 600 μg/rat of AChR were suppressed, while IL‐4, IL‐10 and transforming growth factor‐beta (TGF‐β) mRNA‐expressing cells were not affected. Collectively, these data indicate that nasal administration of AChR in ongoing EAMG induced selective suppression of Th1 functions, i.e. IFN‐γ and IgG2b production, but no influence on Th2 cell functions. The impaired Th1 functions may result in the production of less myasthenic anti‐AChR antibodies and contribute to the amelioration of EAMG severity in rats treated with AChR 600 μg/rat by the nasal route.