Blank, Christian and Gajewski, Thomas F. and Mackensen, Andreas (2005) Interaction of PD-L1 on tumor cells with PD-1 on tumor-specific T cells as a mechanism of immune evasion: implications for tumor immunotherapy. CANCER IMMUNOLOGY IMMUNOTHERAPY, 54 (4). pp. 307-314. ISSN 0340-7004
Full text not available from this repository. (Request a copy)Abstract
Programmed death receptor ligand 1 (PD-L1, also called B7-H1) is a recently described B7 family member. In contrast to B7-1 and B7-2, PD-L1 does not interact with either CD28 or CTLA-4. To date, one specific receptor has been identified that can be ligated by PD-L1. This receptor, programmed death receptor 1 (PD-1), has been shown to negatively regulate T-cell receptor (TCR) signaling. Upon ligating its receptor, PD-L1 has been reported to decrease TCR-mediated proliferation and cytokine production. PD-1 gene-deficient mice developed autoimmune diseases, which early led to the hypothesis of PD-L1 regulating peripheral tolerance. In contrast to normal tissues, which show minimal surface expression of PD-L1 protein, PD-L1 expression was found to be abundant on many murine and human cancers and could be further up-regulated upon IFN-gamma stimulation. Thus, PD-L1 might play an important role in tumor immune evasion. This review discusses the currently available data concerning negative T-cell regulation via PD-1, the blockade of PD-L1/PD-1 interactions, and the implications for adoptive T-cell therapies.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | RECOMBINANT HUMAN INTERLEUKIN-12; PERIPHERAL-BLOOD LYMPHOCYTES; PROGRAMMED DEATH-1; DENDRITIC CELLS; ADOPTIVE TRANSFER; MELANOMA PATIENTS; B7 FAMILY; ANTITUMOR LYMPHOCYTES; POTENTIAL MECHANISM; INHIBITORY RECEPTOR; immune evasion; immunotherapy; PD-L1; T cells; tumor cells |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Innere Medizin III (Hämatologie und Internistische Onkologie) |
| Depositing User: | Petra Gürster |
| Date Deposited: | 23 Mar 2022 06:58 |
| Last Modified: | 23 Mar 2022 06:58 |
| URI: | https://pred.uni-regensburg.de/id/eprint/36286 |
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