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Nasal administration of nicotinic acetycholine receptor (AChR) to Lewis rats prior to myflsthenogenic immunization with Torpedo AChR plus complete Freund’s adjuvant (CFA) resulted in prevention or marked decrease of the severity of experimental autoimmune myasthenia gravis (EAMG), suppression of AChR -specific B cell responses and of AChR- reactive T cell function. To examine the involvement of immunoregtilatory cytokines and the underlying mechanism involved in the induction of nasal tolerance, in situ hybridization with radiolabelled cDNA oligonucleotide probes was adopted to enumerate mononuclear cells (MNC) expressing mRNA for interferon -r (IFN -r), interleukin- 4 and transforming growth factor -β (TGF -β). After coculture with AChR, MNC from certain lymphoid organs examined, mainly from popliteal and inguinal lymph nodes contained higher numbers of IFN - r, IL-4 and TGF - β mRNA expressing cells compared to PBS -administered CFA- injected rats. Nasal tolerance was accompanied by decreased numbe
Nasal administration of nicotinic acetycholine receptor (AChR) to Lewis rats prior to myflsthenogenic immunization with Torpedo AChR plus complete Freund’s adjuvant (CFA) resulted in prevention or marked decrease of severity of experimental autoimmune myasthenia gravis (EAMG), suppression of AChR-specific B cell responses and of AChR-reactive T cell function. To examine the involvement of immunoreglatory cytokines and the underlying mechanism involved in the induction of nasal tolerance, in situ hybridization with radiolabelled cDNA oligonucleotide probes was adopted to enumerate mononuclear cells (MNC) expressing mRNA for After coculture with AChR, MNC from certain lymphoid organs examined, mainly from popliteal and inguinal lymph nodes contained higher numbers of IFN-r , IL-4 and TGF - β mRNA expressing cells compared to PBS-administered CFA-injected rats. Nasal tolerance was accompanied by decreased numbe