Transfer of immune components from rabbit autoimmune cardiomyopathy into severe combined immunodeficiency (SCID) mice induces cardiomyopathic changes

Autor: Mituru Hayase, Michael Fu, Nobuo Yamaguchi, Noboru Takekoshi, Shinobu Matsui, Shogo Katsuda, Kohei Teraoka, Hidekazu Murano, Takayuki Kurihara
Rok vydání: 2006
Předmět:
Zdroj: Autoimmunity. 39:121-128
ISSN: 1607-842X
0891-6934
DOI: 10.1080/08916930500314855
Popis: 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.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-IgGPBL, (beta1+M2)-IgG, (beta1+M2)-PBL, (beta1+M2)-IgGPBL 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)-IgGPBL 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)-IgGPBL group. In the (beta1+M2)-PBL group and (beta1+M2)-IgGPBL group, cardiomyocyte diameters were significantly increased. Some myocytes of the (beta1+M2)-IgGPBL group exhibited intracellular edema, clumps of Z-band and increased numbers of mitochondria by using electron microscopy.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.
Databáze: OpenAIRE
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