Tumor exosomes block dendritic cells maturation to decrease the T cell immune response

Ning, Yongling; Shen, Kai; Wu, Qiyong; Sun, Xiao; Bai, Yu; Xie, Yirui; Pan, Jie; Qi, Chunjian

doi:10.1016/j.imlet.2018.05.002

Cited by 184 publications

(159 citation statements)

References 31 publications

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“…1b). Studies have shown that tumour cell-derived exosomes are involved in multiple immune activities in tumour progression [58,70,71]. In addition, some exosomal RNAs from donor cells, including circRNA, can function in recipient cells [72][73][74].…”

Section: Circrnas Mediate Tumour Immune Surveillancementioning

confidence: 99%

Roles of circRNAs in the tumour microenvironment

et al. 2020

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The tumour microenvironment (TME) constitutes the area surrounding the tumour during its development and has been demonstrated to play roles in cancer-related diseases through crosstalk with tumour cells. Circular RNAs (circRNAs) are a subpopulation of endogenous noncoding RNAs (ncRNAs) that are ubiquitously expressed in eukaryotes and have multiple biological functions in the regulation of cancer onset and progression. An increasing number of studies have shown that circRNAs participate in the multifaceted biological regulation of the TME. However, details on the mechanisms involved have remained elusive until now. In this review, we analyse the effects of circRNAs on the TME from various perspectives, including immune surveillance, angiogenesis, hypoxia, matrix remodelling, exo-circRNAs and chemoradiation resistance. Currently, the enormous potential for circRNA use in targeted therapy and as noninvasive biomarkers have drawn our attention. We emphasize the prospect of targeting circRNAs as an essential strategy to regulate TME, overcome cancer resistance and improve therapeutic outcomes.

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Section: Circrnas Mediate Tumour Immune Surveillancementioning

confidence: 99%

Roles of circRNAs in the tumour microenvironment

et al. 2020

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“…Recent studies show that exosomes released by cancer cells interact amongst others with tumor-infiltrating T cells (TILs) [5], myeloid-derived suppressor cells (MDSCs) or tumor-associated macrophages (TAMs) [6]. They induce a phenotypic switch of tumor-infiltrating immune cells and stroma cells, thereby creating a tumor-permissive microenvironment [7][8][9].…”

Section: Introductionmentioning

confidence: 99%

Melanoma-Derived Exosomal miR-125b-5p Educates Tumor Associated Macrophages (TAMs) by Targeting Lysosomal Acid Lipase A (LIPA)

Gerloff

Luetzkendorf

Moritz

et al. 2020

Cancers

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Tumor-associated macrophages (TAMs) are the most abundant immune cells in the tumor microenvironment, promoting tumor initiation, growth, progression, metastasis, and immune evasion. Recently it was shown that cancer cell-derived exosomes induce a tumor-promoting phenotype in TAMs. Exosome-loaded proteins, DNA, and RNAs may contribute to the macrophage reprogramming. However, the exact mediators and mechanisms, particularly in melanoma, are not known. In this study we examined the effects of cutaneous melanoma-derived exosomes on macrophage function and the underlying mechanisms. First, we showed that exposure to melanoma exosomes induces a tumor-promoting TAM phenotype in macrophages. Sequencing revealed enrichment for several miRNAs including miR-125b-5p in cutaneous melanoma exosomes. We showed that miR-125b-5p is delivered to macrophages by melanoma exosomes and partially induces the observed tumor-promoting TAM phenotype. Finally, we showed that miR-125b-5p targets the lysosomal acid lipase A (LIPA) in macrophages, which in turn contributes to their phenotype switch and promotes macrophage survival. Thus, our data show for the first time that miR-125b-5p transferred by cutaneous melanoma-derived exosomes induces a tumor-promoting TAM phenotype in macrophages.

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“…Moreover, it was reported that TEV-treated DCs failed in inducing CD4+ T cell proliferation and activation, while promoted Treg differentiation. Finally, it has been shown that blockage of PD-L1 partially reversed the immunosuppressive effects induced by TEV-treated DCs [46]. In the lung cancer model, DCs become tolerogenic after incubation with EGFR-enriched TEVs; treated-DCs were then able to induce the generation of immunosuppressive Tregs [47].…”

Section: Tevs and Dendritic Cellsmentioning

confidence: 99%

Extracellular Vesicles and Tumor-Immune Escape: Biological Functions and Clinical Perspectives

Raimondo

Pucci

Alessandro

et al. 2020

IJMS

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The modulation of the immune system is one of the hallmarks of cancer. It is now widely described that cancer cells are able to evade the immune response and thus establish immune tolerance. The exploration of the mechanisms underlying this ability of cancer cells has always attracted the scientific community and is the basis for the development of new promising cancer therapies. Recent evidence has highlighted how extracellular vesicles (EVs) represent a mechanism by which cancer cells promote immune escape by inducing phenotypic changes on different immune cell populations. In this review, we will discuss the recent findings on the role of tumor-derived extracellular vesicles (TEVs) in regulating immune checkpoints, focusing on the PD-L1/PD-1 axis.

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Tumor exosomes block dendritic cells maturation to decrease the T cell immune response

Cited by 184 publications

References 31 publications

Roles of circRNAs in the tumour microenvironment

Roles of circRNAs in the tumour microenvironment

Melanoma-Derived Exosomal miR-125b-5p Educates Tumor Associated Macrophages (TAMs) by Targeting Lysosomal Acid Lipase A (LIPA)

Extracellular Vesicles and Tumor-Immune Escape: Biological Functions and Clinical Perspectives

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