A rheostat for immune responses: the unique properties of PD-1 and their advantages for clinical application
Open Access
- 15 November 2013
- journal article
- review article
- Published by Springer Science and Business Media LLC in Nature Immunology
- Vol. 14 (12), 1212-1218
- https://doi.org/10.1038/ni.2762
Abstract
PD-1, a negative coreceptor expressed on antigen-stimulated T cells and B cells, seems to serve as a 'rheostat' of the immune response. The molecular mechanisms of the functions of PD-1, in conjunction with the mild, chronic and strain-specific autoimmune phenotypes of PD-1-deficient mice, in contrast to the devastating fatal autoimmune disease of mice deficient in the immunomodulatory receptor CTLA-4, suggest that immunoregulation by PD-1 is rather antigen specific and is mainly cell intrinsic. Such unique properties make PD-1 a powerful target for immunological therapy, with highly effective clinical applications for cancer treatment.Keywords
This publication has 91 references indexed in Scilit:
- Safety and Activity of Anti–PD-L1 Antibody in Patients with Advanced CancerThe New England Journal of Medicine, 2012
- Safety, Activity, and Immune Correlates of Anti–PD-1 Antibody in CancerThe New England Journal of Medicine, 2012
- Chronic Virus Infection Enforces Demethylation of the Locus that Encodes PD-1 in Antigen-Specific CD8+ T CellsImmunity, 2011
- Follicular regulatory T cells expressing Foxp3 and Bcl-6 suppress germinal center reactionsNature Medicine, 2011
- Foxp3+ follicular regulatory T cells control the germinal center responseNature Medicine, 2011
- PD-1 regulates germinal center B cell survival and the formation and affinity of long-lived plasma cellsNature Immunology, 2010
- Severe functional impairment and elevated PD‐1 expression in CD1d‐restricted NKT cells retained during chronic HIV‐1 infectionEuropean Journal of Immunology, 2009
- TGF-β: A Master of All T Cell TradesCell, 2008
- The PD-1/PD-L1 complex resembles the antigen-binding Fv domains of antibodies and T cell receptorsProceedings of the National Academy of Sciences of the United States of America, 2008
- Targeted disruption of the mouse transforming growth factor-β1 gene results in multifocal inflammatory diseaseNature, 1992