Autoantibodies against cardiac troponin I are responsible for dilated cardiomyopathy in PD-1-deficient mice

被引：0

作者：

Taku Okazaki

Yoshimasa Tanaka

Ryosuke Nishio

Tamotsu Mitsuiye

Akira Mizoguchi

Jian Wang

Masayoshi Ishida

Hiroshi Hiai

Akira Matsumori

Nagahiro Minato

Tasuku Honjo

机构：

[1] Graduate School of Medicine,Department of Medical Chemistry and Molecular Biology

[2] Kyoto University,Department of Immunology and Cell Biology

[3] Yoshida-Konoe,Department of Cardiovascular Medicine

[4] Sakyo-ku,Division of Emergency Medicine

[5] Graduate School of Biostudies,Department of Physiology and Biophysics

[6] Kyoto University,Department of Anatomy

[7] Yoshida-Konoe,Department of Pathology and Biology of Diseases

[8] Sakyo-ku,undefined

[9] Precursory Research for Embryonic Science and Technology (PRESTO),undefined

[10] Japan Science and Technology Agency (JST),undefined

[11] 4-1-8 Honcho Kawaguchi,undefined

[12] Graduate School of Medicine,undefined

[13] Kyoto University,undefined

[14] Yoshida-Konoe,undefined

[15] Sakyo-ku,undefined

[16] Kyoto University Hospital,undefined

[17] Shogoin-Kawahara-cho,undefined

[18] Sakyo-ku,undefined

[19] Graduate School of Medicine,undefined

[20] Kyoto University,undefined

[21] Yoshida-Konoe,undefined

[22] Sakyo-ku,undefined

[23] Graduate School of Medicine,undefined

[24] Mie University,undefined

[25] Edobashi,undefined

[26] Graduate School of Medicine,undefined

[27] Kyoto University,undefined

[28] Yoshida-Konoe,undefined

[29] Sakyo-ku,undefined

来源：

Nature Medicine | 2003年 / 9卷

关键词：

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学科分类号：

摘要：

We recently reported that mice deficient in the programmed cell death-1 (PD-1) immunoinhibitory coreceptor develop autoimmune dilated cardiomyopathy (DCM), with production of high-titer autoantibodies against a heart-specific, 30-kDa protein. In this study, we purified the 30-kDa protein from heart extract and identified it as cardiac troponin I (cTnI), encoded by a gene in which mutations can cause familial hypertrophic cardiomyopathy (HCM). Administration of monoclonal antibodies to cTnI induced dilatation and dysfunction of hearts in wild-type mice. Monoclonal antibodies to cTnI stained the surface of cardiomyocytes and augmented the voltage-dependent L-type Ca2+ current of normal cardiomyocytes. These findings suggest that antibodies to cTnI induce heart dysfunction and dilatation by chronic stimulation of Ca2+ influx in cardiomyocytes.

引用

页码：1477 / 1483

页数：6

共 50 条

[1] Autoantibodies against cardiac troponin I are responsible for dilated cardiomyopathy in PD-1-deficient mice
Okazaki, T
Tanaka, Y
Nishio, R
Mitsuiye, T
Mizoguchi, A
Wang, J
Ishida, M
Hiai, H
Matsumori, A
Minato, N
Honjo, T
[J]. NATURE MEDICINE, 2003, 9 (12) : 1477 - 1483
[2] Left ventricular pressure-volume relationship and the role of autuantibodies against cardiac troponin I in PD-1-deficient mice with dilated cardiomyopathy
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[J]. JOURNAL OF CARDIAC FAILURE, 2004, 10 (05) : S161 - S161
[3] The role of autoantibodies against cardiac troponin I in autoimmune dilated cardiomyopathy
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[4] Autoantibodies against cardiac troponin I in patients with dilated cardiomyopathy predict improvement of cardiac function by immunoadsorption
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[10] Impact of Troponin I-Autoantibodies in Chronic Dilated and Ischemic Cardiomyopathy
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