scholarly journals Exosomal PD-L1: New Insights Into Tumor Immune Escape Mechanisms and Therapeutic Strategies

2020 ◽  
Vol 8 ◽  
Author(s):  
Kaijian Zhou ◽  
Shu Guo ◽  
Fei Li ◽  
Qiang Sun ◽  
Guoxin Liang
Keyword(s):  
Immune Escape ◽  
Therapeutic Strategies ◽  
Tumor Immune Escape ◽  
Immune Escape Mechanisms

scholarly journals Implications of Corticotropin Releasing Factor in Targeted Anticancer Therapy

2010 ◽  
Vol 23 (2) ◽  
pp. 86-90 ◽  
Author(s):  
Byung-Jin Kim ◽  
Harlan P. Jones
Keyword(s):  
Side Effects ◽  
Immune Escape ◽  
Anticancer Therapy ◽  
Corticotropin Releasing Factor ◽  
Antitumor Therapy ◽  
Tumor Immune Escape ◽  
Adverse Side Effects ◽  
Psychological Indicators ◽  
Immune Escape Mechanisms

There is a need to develop novel anticancer therapies that eliminate adverse side effects produced by current treatments. Corticotropin releasing factor (CRF), an endogenous neuroedocrine factor, which typically regulates biological and psychological indicators of stress, has recently been found to be expressed by tumor malignancies. Here, we discuss the implications of CRF as a target for antitumor therapy through regulation of tumor immune escape mechanisms.

scholarly journals The role of tumor-derived exosomes in tumor immune escape: A concise review

2020 ◽  
Vol 7 (11) ◽  
pp. 4132-4137
Author(s):  
Nhat Chau Truong ◽  
Thao Nhi Huynh ◽  
Khuong Duy Pham ◽  
Phuc Van Pham
Keyword(s):  
Immune Modulation ◽  
Immune Escape ◽  
Suppressor Cells ◽  
Target Cells ◽  
Myeloid Derived Suppressor Cells ◽  
Tumor Immune Escape ◽  
Concise Review ◽  
Viable Cells ◽  
Immune Escape Mechanisms

Exosomes are small vesicles secreted by viable cells into the microenvironment. These vesicles bring various compositions, including lipids, RNAs and proteins, which carry information from producer cells to target cells. Cancer cells also produce exosomes, termed as tumor-derived exosomes (TDEs), which play important roles in immune modulation, angiogenesis and metastasis of tumors. This review summarizes the roles of TDEs in tumor immune escape mechanisms. TDEs affect all kinds of tumor-associated immune cells, including natural killer (NK) cells, dendritic cells (DCs), T and B lymphocytes, and myeloid-derived suppressor cells (MDSCs). Generally, TDEs suppress the immune system to promote tumor immune escape, thereby significantly contributing to tumorigenesis and metastasis.

scholarly journals Leveraging NKG2D Ligands in Immuno-Oncology

2021 ◽  
Vol 12 ◽  
Author(s):  
Mercedes Beatriz Fuertes ◽  
Carolina Inés Domaica ◽  
Norberto Walter Zwirner
Keyword(s):  
Cell Surface ◽  
Nk Cells ◽  
Immune Escape ◽  
Nk Cell ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Combination Therapies ◽  
Tumor Immune Escape ◽  
Effector Functions ◽  
Immune Escape Mechanisms

Immune checkpoint inhibitors (ICI) revolutionized the field of immuno-oncology and opened new avenues towards the development of novel assets to achieve durable immune control of cancer. Yet, the presence of tumor immune evasion mechanisms represents a challenge for the development of efficient treatment options. Therefore, combination therapies are taking the center of the stage in immuno-oncology. Such combination therapies should boost anti-tumor immune responses and/or target tumor immune escape mechanisms, especially those created by major players in the tumor microenvironment (TME) such as tumor-associated macrophages (TAM). Natural killer (NK) cells were recently positioned at the forefront of many immunotherapy strategies, and several new approaches are being designed to fully exploit NK cell antitumor potential. One of the most relevant NK cell-activating receptors is NKG2D, a receptor that recognizes 8 different NKG2D ligands (NKG2DL), including MICA and MICB. MICA and MICB are poorly expressed on normal cells but become upregulated on the surface of damaged, transformed or infected cells as a result of post-transcriptional or post-translational mechanisms and intracellular pathways. Their engagement of NKG2D triggers NK cell effector functions. Also, MICA/B are polymorphic and such polymorphism affects functional responses through regulation of their cell-surface expression, intracellular trafficking, shedding of soluble immunosuppressive isoforms, or the affinity of NKG2D interaction. Although immunotherapeutic approaches that target the NKG2D-NKG2DL axis are under investigation, several tumor immune escape mechanisms account for reduced cell surface expression of NKG2DL and contribute to tumor immune escape. Also, NKG2DL polymorphism determines functional NKG2D-dependent responses, thus representing an additional challenge for leveraging NKG2DL in immuno-oncology. In this review, we discuss strategies to boost MICA/B expression and/or inhibit their shedding and propose that combination strategies that target MICA/B with antibodies and strategies aimed at promoting their upregulation on tumor cells or at reprograming TAM into pro-inflammatory macrophages and remodeling of the TME, emerge as frontrunners in immuno-oncology because they may unleash the antitumor effector functions of NK cells and cytotoxic CD8 T cells (CTL). Pursuing several of these pipelines might lead to innovative modalities of immunotherapy for the treatment of a wide range of cancer patients.

scholarly journals Cross-platform meta-analysis reveals common matrisome variation associated with tumor genotypes and immunophenotypes in human cancers

2018 ◽  
Author(s):  
Su Bin Lim ◽  
Swee Jin Tan ◽  
Wan-Teck Lim ◽  
Chwee Teck Lim
Keyword(s):  
Immune Cell ◽  
Immune Escape ◽  
Wide Spectrum ◽  
Meta Analysis ◽  
Immune Checkpoints ◽  
Tumor Immune Escape ◽  
Data Resource ◽  
Specific Tumor ◽  
Cross Platform ◽  
Immune Escape Mechanisms

AbstractBackgroundRecent sequencing efforts unveil genomic landscapes of the tumor microenvironment. Yet, little is known about the extent to which matrisome pattern is conserved in progressive tumors across diverse cancer types, and thus its clinical impact remains largely unexplored.FindingsUsing a newly generated, unified data resource, we conducted cross-platform assessment of a measure of altered extra-cellular matrix (ECM) composition and remodeling associated with tumor progression, termed as the matrisome index (TMI). Parallel analyses with TCGA in over 30,000 patient-derived biopsies revealed that TMI is closely associated with mutational load, tumor histopathology, and predictive of patient outcomes. We found an enrichment of specific tumor-infiltrating immune cell populations, signatures predictive of immunotherapy resistance, and several immune checkpoints in tumors with high TMI, suggesting potential role of ECM interaction with immunophenotyes and tumor immune escape mechanisms. Both epithelial cancer cells and carcinoma-associated fibroblasts are potential cellular contributors of such deregulated matrisome.ConclusionsDespite wide spectrum of genetic heterogeneity and dynamic nature, matrisome abnormalities are integral to disease progression. Our resource of a curated compendium of 8,386 genome-wide profiles, molecular and clinical associations, and matrisome-tumor genotype-immunophenotype relationships identify potentially actionable immune targets that may guide personalized immunotherapy.

Tumor Immune Escape Mechanisms

2007 ◽  
pp. 577-602 ◽  
Author(s):  
Yi Ting Koh ◽  
M. Luz García-Hernández ◽  
W. Martin Kast
Keyword(s):  
Immune Escape ◽  
Tumor Immune Escape ◽  
Immune Escape Mechanisms

Does mistletoe interact with tumor immune-escape mechanisms?

Phytomedicine ◽  
2019 ◽  
Vol 61 ◽  
pp. 5
Author(s):  
Amy Marisa Zimmermann-Klemd ◽  
Seema Devi ◽  
Carmen Steinborn ◽  
Konrad Urech ◽  
Roman Huber ◽  
...  
Keyword(s):  
Immune Escape ◽  
Tumor Immune Escape ◽  
Immune Escape Mechanisms
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