title: Antigen-specific immunosuppression: nasal tolerance to P0 protein peptides for the prevention and treatment of experimental autoimmune neuritis in Lewis rats.
abstract: Experimental autoimmune neuritis (EAN) is an autoimmune inflammatory demyelinating disease of the peripheral nervous system (PNS), and represents an animal model of the human Guillain-Barré syndrome (GBS). In this study, we report that nasal administration of the neuritogenic peptide 180-199 and of the cryptic peptide 56-71 of the rat neuritogenic P0 protein of peripheral nerve myelin prevents EAN and attenuates ongoing EAN. Both peptides effectively decreased the severity and shortened clinical EAN. Both a prophylactic and a therapeutic approach proved to be beneficial. These effects were associated with T and B cells hyporesponsiveness to the peptide antigens, reflected by downregulated Th1 cell responses (interferon-gamma secretion) and macrophage function, whereas Th2 cell responses (IL-4 secretion) and transforming growth factor-beta mRNA expression were upregulated.
authors.affiliation: Division of Neurology, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden.
authors.forename: L P
authors.initials: LP
authors.lastname: Zou
authors.forename: D H
authors.initials: DH
authors.lastname: Ma
authors.forename: M
authors.initials: M
authors.lastname: Levi
authors.forename: B
authors.initials: B
authors.lastname: Wahren
authors.forename: L
authors.initials: L
authors.lastname: Wei
authors.forename: E
authors.initials: E
authors.lastname: Mix
authors.forename: P H
authors.initials: PH
authors.lastname: van der Meide
authors.forename: H
authors.initials: H
authors.lastname: Link
authors.forename: J
authors.initials: J
authors.lastname: Zhu
mesh_terms: D000281:Administration, Intranasal; D000818:Animals; D001402:B-Lymphocytes / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D002417:Cattle; D004195:Disease Models, Animal; D000939:Epitopes; D015870:Gene Expression / Q000276:immunology; D000949:Histocompatibility Antigens Class II / Q000378:metabolism; D007114:Immunization; D007074:Immunoglobulin G / Q000276:immunology; D007165:Immunosuppression Therapy; D007371:Interferon-gamma / Q000378:metabolism; D015847:Interleukin-4 / Q000378:metabolism; D008198:Lymph Nodes / Q000276:immunology; D008297:Male; D018993:Myelin P0 Protein / Q000276:immunology* / Q000494:pharmacology*; D009444:Neuritis, Autoimmune, Experimental / Q000188:drug therapy / Q000276:immunology* / Q000517:prevention & control*; D010446:Peptide Fragments / Q000494:pharmacology; D011129:Polyradiculoneuropathy / Q000188:drug therapy / Q000276:immunology / Q000517:prevention & control; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D011917:Rats, Inbred Lew; D012584:Sciatic Nerve / Q000737:chemistry / Q000276:immunology; D016212:Transforming Growth Factor beta / Q000235:genetics
chemical_list: D000939:Epitopes; D000949:Histocompatibility Antigens Class II; D007074:Immunoglobulin G; D018993:Myelin P0 Protein; D010446:Peptide Fragments; D012333:RNA, Messenger; D016212:Transforming Growth Factor beta; D015847:Interleukin-4; D007371:Interferon-gamma