title: Effects of antineuronal antibodies from patients with paraneoplastic neurological syndrome on primary-cultured neurons.
abstract: Some patients with paraneoplastic neurological syndrome (PNS) produce autoantibodies against tumor and neuronal tissues of symptom-relevant areas. These characteristic antibodies are detected at early stages of the neurological disorder and are reliable markers for the diagnosis of PNS and underlying cancers. These antibodies are thought to be related directly to neuronal damage. However, the passive transfer of antibodies to rodents has been succeeded only in those in which the target antigens were expressed on the cell surface, like Lambert-Eaton myasthenic syndrome. The serum IgGs from patients with PNS and anti-Yo or anti-Hu antibody were not shown to induce the disease by passive transfer or active immunization with these antigen proteins to date. Instead, cytotoxic T lymphocytes (CTLs) against these antigen peptides-presenting targets could be induced in the peripheral blood of PNS patients. However, there is no direct proof of CTLs killing neurons. In this study, we examined the effects of the anti-Yo or anti-Hu antibody on mouse-brain-derived neurons in a primary culture system and found that these antibodies did not kill neurons, but induced the expression of cell adhesion molecules and accelerated neuronal differentiation. These effects of serum IgG fractions containing the anti-Yo or the anti-Hu antibody on the cultured neurons were the same, suggesting that their effects were not through the binding of the antibody to specific antigens, but to some other factors contained in IgG fractions.
authors.affiliation: Department of Neurology, Brain Research Institute, Niigata University, 1-757 Asahimachi-dori, Niigata 951-8585, Japan. keiko@bri.niigata-u.ac.jp
authors.forename: Keiko
authors.initials: K
authors.lastname: Tanaka
authors.forename: Xin
authors.initials: X
authors.lastname: Ding
authors.forename: Masami
authors.initials: M
authors.lastname: Tanaka
mesh_terms: D000818:Animals; D000906:Antibodies / Q000378:metabolism / Q000494:pharmacology*; D002454:Cell Differentiation / Q000187:drug effects; D002478:Cells, Cultured; D005576:Colforsin / Q000494:pharmacology; D000242:Cyclic AMP / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000276:immunology; D004305:Dose-Response Relationship, Drug; D051959:ELAV Proteins; D004622:Embryo, Mammalian; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000378:metabolism / Q000494:pharmacology; D007150:Immunohistochemistry; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009363:Neoplasm Proteins / Q000276:immunology; D009419:Nerve Tissue Proteins / Q000276:immunology; D009474:Neurons / Q000187:drug effects*; D020361:Paraneoplastic Syndromes, Nervous System / Q000276:immunology*; D011247:Pregnancy; D016601:RNA-Binding Proteins / Q000276:immunology; D013936:Thymidine / Q000378:metabolism; D013997:Time Factors; D014316:Tritium / Q000378:metabolism
chemical_list: D000906:Antibodies; C095184:CDR2 protein, human; D004268:DNA-Binding Proteins; D051959:ELAV Proteins; D007074:Immunoglobulin G; D009363:Neoplasm Proteins; D009419:Nerve Tissue Proteins; D016601:RNA-Binding Proteins; D014316:Tritium; D005576:Colforsin; D000242:Cyclic AMP; D013936:Thymidine