Trial to establish an animal model of paraneoplastic cerebellar degeneration with anti-Yo antibody. 2. Passive transfer of murine mononuclear cells activated with recombinant Yo protein to paraneoplastic cerebellar degeneration lymphocytes in severe combined immunodeficiency mice.
Passive transfer of serum IgG or mononuclear cells from peripheral blood of a patient with paraneoplastic cerebellar degeneration (PCD) to rodents was carried out in order to examine the role of anti-Purkinje cell antibody (anti-Yo antibody) present in serum and cerebrospinal fluid of PCD patients. After a single injection of IgG into mouse brain, it was taken up by Purkinje cells and remained there for more than 36 h without Purkinje cell loss. Injection of PCD IgG together with complement or lipopolysaccharide-activated human macrophages or rat mononuclear cells into rat ventricles did not cause Purkinje cell loss. We also studied passive transfer of the PCD patient's lymphocytes to mice with severe combined immunodeficiency (SCID). We constructed a recombinant Yo fusion protein that has the leucine-zipper protein (Yo protein), the common epitope for anti-Yo antibody for immunizing mice, and that resulted in production of significant amounts of anti-Yo antibody. Spleen cells from these Yo protein immunized mice were injected intravenously or intracerebrally into naive mice that subsequently showed no neurological symptoms or loss of Purkinje cells. We conclude that the anti-Yo antibody, either in combination with or without complement or activated mononuclear cells, cannot be the sole cause of Purkinje cell loss.
Tanaka
K
K
Department of Neurology, Brain Research Institute, Niigata University, Japan.
Tanaka
M
M
Igarashi
S
S
Onodera
O
O
Miyatake
T
T
Tsuji
S
S
D000230:Adenocarcinoma / Q000276:immunology / Q000473:pathology; D000368:Aged; D000818:Animals; D001323:Autoantibodies / Q000032:analysis*; D001324:Autoantigens; D001402:B-Lymphocytes / Q000276:immunology; D001921:Brain / Q000276:immunology / Q000473:pathology; D002524:Cerebellar Ataxia / Q000276:immunology / Q000473:pathology; D002526:Cerebellar Diseases / Q000276:immunology* / Q000473:pathology; D004268:DNA-Binding Proteins / Q000276:immunology*; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D005185:Fallopian Tube Neoplasms / Q000276:immunology / Q000473:pathology; D005260:Female; D006801:Humans; D007116:Immunization, Passive; D008213:Lymphocyte Activation / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D016513:Mice, SCID; D009363:Neoplasm Proteins / Q000276:immunology*; D009410:Nerve Degeneration / Q000276:immunology*; D009419:Nerve Tissue Proteins; D010257:Paraneoplastic Syndromes / Q000276:immunology* / Q000473:pathology; D011689:Purkinje Cells / Q000276:immunology / Q000473:pathology; D051381:Rats; D011994:Recombinant Proteins / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology
D001323:Autoantibodies; D001324:Autoantigens; C063762:CDR1 protein, human; C095184:CDR2 protein, human; D004268:DNA-Binding Proteins; D009363:Neoplasm Proteins; D009419:Nerve Tissue Proteins; D011994:Recombinant Proteins