title: Transfer of immune components from rabbit autoimmune cardiomyopathy into severe combined immunodeficiency (SCID) mice induces cardiomyopathic changes.
abstract: BACKGROUND
  Growing evidence suggests that autoimmune mechanism plays an important role in the pathogenesis of cardiomyopathy. The purpose of this study was to investigate whether passive transfer of IgG and/or lymphocytes from rabbits with autoimmune cardiomyopathy is able to reproduce cardiomyopathic changes in severe combined immunodeficiency (SCID) mice.
  
  
  RESULTS
  SCID mice were injected intraperitoneally with IgG and/or peripheral blood lymphocytes (PBL) from either rabbits immunized with both beta1-adrenoceptor peptide and M2-muscarinic receptor peptide (beta1+M2 group) or rabbits with adjuvant (N group). Thirty five SCID mice were divided into seven groups; N-IgG, N-PBL, N-IgG & PBL, (beta1+M2)-IgG, (beta1+M2)-PBL, (beta1+M2)-IgG & PBL and control groups. Heart weight in three (beta1+M2) groups were significantly increased. All mice in three (beta1+M2) groups showed high titer of rabbit anti-beta1 adrenoceptor autoantibodies, and 4 mice in the (beta1+M2)-PBL group and 3 mice in the (beta1+M2)-IgG & PBL group showed a significant increase in titer of rabbit anti-M2-muscarinic receptor autoantibodies. Focal infiltration of inflammatory cells in the myocardium was observed in the (beta1+M2)-IgG & PBL group. In the (beta1+M2)-PBL group and (beta1+M2)-IgG & PBL group, cardiomyocyte diameters were significantly increased. Some myocytes of the (beta1+M2)-IgG & PBL group exhibited intracellular edema, clumps of Z-band and increased numbers of mitochondria by using electron microscopy.
  
  
  CONCLUSIONS
  Transfer of IgG and PBL from rabbits immunized with combined beta1 and M2 peptides was able to reproduce the early stage of cardiomyopathic changes in SCID mice.
authors.affiliation: Kanazawa Medical University, Department of Cardiology, Uchinada, Ishikawa, Japan. matsui@kanazawa-med.ac.jp
authors.forename: Shinobu
authors.initials: S
authors.lastname: Matsui
authors.forename: Michael
authors.initials: M
authors.lastname: Fu
authors.forename: Mituru
authors.initials: M
authors.lastname: Hayase
authors.forename: Shogo
authors.initials: S
authors.lastname: Katsuda
authors.forename: Nobuo
authors.initials: N
authors.lastname: Yamaguchi
authors.forename: Kohei
authors.initials: K
authors.lastname: Teraoka
authors.forename: Takayuki
authors.initials: T
authors.lastname: Kurihara
authors.forename: Hidekazu
authors.initials: H
authors.lastname: Murano
authors.forename: Noboru
authors.initials: N
authors.lastname: Takekoshi
mesh_terms: D000595:Amino Acid Sequence; D000818:Animals; D001327:Autoimmune Diseases / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D009202:Cardiomyopathies / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D005260:Female; D006801:Humans; D007114:Immunization; D007116:Immunization, Passive; D008297:Male; D051379:Mice; D016513:Mice, SCID; D008854:Microscopy, Electron; D008969:Molecular Sequence Data; D010446:Peptide Fragments / Q000235:genetics / Q000276:immunology; D011817:Rabbits; D043585:Receptor, Muscarinic M2 / Q000235:genetics / Q000276:immunology; D018342:Receptors, Adrenergic, beta-1 / Q000235:genetics / Q000276:immunology; D011994:Recombinant Proteins / Q000235:genetics / Q000276:immunology
chemical_list: D010446:Peptide Fragments; D043585:Receptor, Muscarinic M2; D018342:Receptors, Adrenergic, beta-1; D011994:Recombinant Proteins