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

By Taku Okazaki, Yoshimasa Tanaka, R. Nishio, T. Mitsuiye, A. Mizoguchi, Jian Wang, Masayoshi Ishida, H. Hiai, A. Matsumori, N. Minato and 1 more. Nature Medicine, 2003

681 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/8b8bf12ad1a303d244e325c58410b356c4ed2945

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

1. Lieping Chen
2. M. Keir
3. M. Butte
4. W. Zou
5. D. Pardoll
6. E. Buchbinder
7. Arlene H. Sharpe
8. A. Schietinger

Citations in the corpus

• Co-inhibitory molecules of the B7–CD28 family in the control of T-cell immunity (2004, background): “Affected hearts have deposits of IgG on the surface of cardiomyocytes, and the affected Pd1-deficient mice have a high serum titre of an IgG autoantibody specific for cardiac troponin I protei”
• PD-1 and its ligands in tolerance and immunity. (2008, background): “Pdcd1−/− Balb/c mice develop a dilated cardiomyopathy owing to the production of an autoantibody against cardiac troponin (6, 54).”
• Targeting the PD-1/B7-H1(PD-L1) pathway to activate anti-tumor immunity (2012, neutral): “Knockout mice develop late-onset, strain specific autoimmunity; on a C57/Bl6 background this manifests as sporadic glomerulonephritis [28], on a Balb/c background as an antibody-mediated cardiomyopathy [29].”