PD-L1

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منابع مشابه

Regulation of PD-1/PD-L1 pathway and resistance to PD-1/PD-L1 blockade

Immune checkpoint blockades, such as inhibitors against programmed death 1 (PD-1) and its ligand (PD-L1), have received extensive attention in the past decade because of their dramatic clinical outcomes in advanced malignancies. However, both primary and acquired resistance becomes one of the major obstacles, which greatly limits the long-lasting effects and wide application of PD-1/PD-L1 block...

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Macrophage PD-L1 strikes back: PD-1/PD-L1 interaction drives macrophages toward regulatory subsets

Activated macrophages have been simply defined as cells that secrete inflammatory mediators and kill intracellular pathogens until few years ago. Recent studies have proposed a new classification system to separate activated macrophages based on their functional phenotypes: host defense, wound healing, and immune regulation. Regulatory macrophages can arise following innate or adaptive immune r...

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PD-L1, Inflammation and Glioblastoma

The PD-L1 protein has an extracellular domain, a transmembrane domain and an intracellular domain. The extracellular domain (ECD) of the PD-L1 protein is comprised of IgC–like and IgV-like domains [2]. The ECD of PD-L1 interacts with the programmed death 1 (PD-1, also known as PDCD1) and B7.1 receptors. Blocking of the PD-L1 molecule with antibodies blocks cancer cells from killing cytotoxic T ...

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Host expression of PD-L1 determines efficacy of PD-L1 pathway blockade-mediated tumor regression.

Programmed death-1 receptor (PD-L1, B7-H1) and programmed cell death protein 1 (PD-1) pathway blockade is a promising therapy for treating cancer. However, the mechanistic contribution of host and tumor PD-L1 and PD-1 signaling to the therapeutic efficacy of PD-L1 and PD-1 blockade remains elusive. Here, we evaluated 3 tumor-bearing mouse models that differ in their sensitivity to PD-L1 blockad...

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ژورنال

عنوان ژورنال: Journal of Clinical Pathology

سال: 2017

ISSN: 0021-9746,1472-4146

DOI: 10.1136/jclinpath-2017-204853