期刊
INTERNATIONAL JOURNAL OF CLINICAL ONCOLOGY
卷 21, 期 3, 页码 448-455出版社
SPRINGER JAPAN KK
DOI: 10.1007/s10147-016-0958-0
关键词
PD-1; CTLA-4; Immune checkpoint blockade; Immune tolerance; Costimulation; T lymphocytes
类别
资金
- JSPS [25460363]
- Grants-in-Aid for Scientific Research [25460363, 16K08847] Funding Source: KAKEN
Successful cancer treatment requires understanding host immune response against tumor cells. PD-1 belongs to the CD28 superfamily of receptors that work as checkpoints of immune activation. PD-1 maintains immune self-tolerance to prevent autoimmunity and controls T-cell reaction during infection to prevent excessive tissue damage. Tumor cells that arise from normal tissue acquire mutations that can be targeted by lymphocytes. Accumulating lines of evidence suggest that tumor cells evade host immune attack by expressing physiological PD-1 ligands and stimulating PD-1 on the lymphocytes. Based on this idea, researchers have successfully demonstrated that systemic administration of monoclonal antibodies that inhibit the binding of PD-1 to the ligands reactivated T cells and augmented the anti-cancer immune response. In this review, I summarize the basics of T-cell biology and its regulation by PD-1 and discuss the current understanding and questions about this multifaceted molecule.
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