A rheostat for immune responses: the unique properties of PD-1 and their advantages for clinical application-Reference-Cited by-同舟云学术

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A rheostat for immune responses: the unique properties of PD-1 and their advantages for clinical application

Published:2013-11-15 Issue:12 Volume:14 Page:1212-1218
ISSN:1529-2908
Container-title:Nature Immunology
language:en
Short-container-title:Nat Immunol

Author:

Okazaki Taku,Chikuma Shunsuke,Iwai Yoshiko,Fagarasan Sidonia,Honjo Tasuku

Publisher

Springer Science and Business Media LLC

Subject

Immunology,Immunology and Allergy

Link

http://www.nature.com/articles/ni.2762.pdf

Reference90 articles.

1. Ishida, Y., Agata, Y., Shibahara, K. & Honjo, T. Induced expression of PD-1, a novel member of the immunoglobulin gene superfamily, upon programmed cell death. EMBO J. 11, 3887–3895 (1992).Original report of the isolation and characterization of mouse PD-1 by subtractive cDNA library between stimulated and control thymoma cell lines; PD-1 was induced on mouse thymoma cell lines treated with apoptotic stimuli.

2. Nishimura, H., Nose, M., Hiai, H., Minato, N. & Honjo, T. Development of lupus-like autoimmune diseases by disruption of the PD-1 gene encoding an ITIM motif-carrying immunoreceptor. Immunity 11, 141–151 (1999).First demonstration that C57BL/6 Pdcd1−/− mice succumb to systemic lupus erythematosus–like autoimmune manifestations; these data indicated a crucial role for PD-1 in maintaining self-tolerance.

3. Nishimura, H. et al. Autoimmune dilated cardiomyopathy in PD-1 receptor-deficient mice. Science 291, 319–322 (2001).First report showing that Pdcd1−/− mice on the BALB/c background develop lethal dilated cadiomyopathy; together with ref. 2 , this paper revealed that PD-1 deficiency results in an autoimmune reaction to different organs, depending on the genetic background.

4. Wang, J. et al. Establishment of NOD-Pdcd1−/− mice as an efficient animal model of type I diabetes. Proc. Natl. Acad. Sci. USA 102, 11823–11828 (2005).

5. Wang, J. et al. PD-1 deficiency results in the development of fatal myocarditis in MRL mice. Int. Immunol. 22, 443–452 (2010).

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