Recruitment and Expansion of Tregs Cells in the Tumor Environment—How to Target Them?

Cinier, Justine; Hubert, Margaux; Besson, Laurie; Roio, Anthony Di; Rodriguez, Céline; Lombardi, Vincent; Caux, Christophe; Ménétrier‐Caux, Christine

doi:10.3390/cancers13081850

Cited by 53 publications

(55 citation statements)

References 394 publications

(308 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The activation of Treg cells is antigen-specific, which implies that the suppressive activity of Treg cells is triggered in an antigen-specific fashion. In cancer, there has been a strong correlation between the frequencies of Treg cells in the TME and anti-tumor immunosuppression [16].…”

Section: Cd4 and Cd8 T Cellsmentioning

confidence: 99%

Regulation of T Cells in Cancer by Nitric Oxide

Navasardyan

Bonavida

2021

Cells

View full text Add to dashboard Cite

The T cell-mediated immune response is primarily involved in the fight against infectious diseases and cancer and its underlying mechanisms are complex. The anti-tumor T cell response is regulated by various T cell subsets and other cells and tissues in the tumor microenvironment (TME). Various mechanisms are involved in the regulation of these various effector cells. One mechanism is the iNOS/.NO that has been reported to be intimately involved in the regulation and differentiation of the various cells that regulate the anti-tumor CD8 T cells. Both endogenous and exogenous .NO are implicated in this regulation. Importantly, the exposure of T cells to .NO had different effects on the immune response, depending on the .NO concentration and time of exposure. For instance, iNOS in T cells regulates activation-induced cell death and inhibits Treg induction. Effector CD8 T cells exposed to .NO result in the upregulation of death receptors and enhance their anti-tumor cytotoxic activity. .NO-Tregs suppress CD4 Th17 cells and their differentiation. Myeloid-derived suppressor cells (MDSCs) expressing iNOS inhibit T cell functions via .NO and inhibit anti-tumor CD8 T cells. Therefore, both .NO donors and .NO inhibitors are potential therapeutics tailored to specific target cells that regulate the T cell effector anti-tumor response.

show abstract

Section: Cd4 and Cd8 T Cellsmentioning

confidence: 99%

Regulation of T Cells in Cancer by Nitric Oxide

Navasardyan

Bonavida

2021

Cells

View full text Add to dashboard Cite

show abstract

“…Its ligand CCL20 is broadly produced by epithelial cells, endothelial cells, and several immune cells such as Th17 cells, B cells, NK cells, and neutrophils [ 127 , 180 , 181 ]. The expression of CCL20 has been reported to be increased in tumor tissues of many types of cancer including breast cancer, colon cancer, skin cancer, oral cancer, and prostate cancer [ 127 , 182 ]. CCL20 is also frequently expressed by various types of cancer including hepatocellular carcinoma, breast cancer, colon cancer, pancreatic cancer, prostate cancer, lung cancer, and renal cell carcinoma [ 127 , 180 , 181 ].…”

Section: Treg Cellmentioning

confidence: 99%

Multifaceted Roles of Chemokines and Chemokine Receptors in Tumor Immunity

Matsuo

Yoshie

Nakayama

2021

Cancers

View full text Add to dashboard Cite

Various immune cells are involved in host tumor immune responses. In particular, there are many T cell subsets with different roles in tumor immunity. T-helper (Th) 1 cells are involved in cellular immunity and thus play the major role in host anti-tumor immunity by inducing and activating cytotoxic T lymphocytes (CTLs). On the other hand, Th2 cells are involved in humoral immunity and suppressive to Th1 responses. Regulatory T (Treg) cells negatively regulate immune responses and contribute to immune evasion of tumor cells. Th17 cells are involved in inflammatory responses and may play a role in tumor progression. However, recent studies have also shown that Th17 cells are capable of directly inducting CTLs and thus may promote anti-tumor immunity. Besides these T cell subsets, there are many other innate immune cells such as dendritic cells (DCs), natural killer (NK) cells, and myeloid-derived suppressor cells (MDSCs) that are involved in host immune responses to cancer. The migratory properties of various immune cells are critical for their functions and largely regulated by the chemokine superfamily. Thus, chemokines and chemokine receptors play vital roles in the orchestration of host immune responses to cancer. In this review, we overview the various immune cells involved in host responses to cancer and their migratory properties regulated by the chemokine superfamily. Understanding the roles of chemokines and chemokine receptors in host immune responses to cancer may provide new therapeutic opportunities for cancer immunotherapy.

show abstract

“…T regs are already detected in, or near early PanINs. Their numbers expand with PDAC progression and elevated levels were associated with bad prognosis for patients [ 7 , 145 ]. A recent study showed that the increased number of T regs is partly caused by PDAC-sEVs that foster T reg expansion by enhanced expression of FOXP3 [ 146 ].…”

Section: Sev-mediated Crosstalk Of Pdac and Associated Cells In The Tmementioning

confidence: 99%

Pancreatic Cancer Small Extracellular Vesicles (Exosomes): A Tale of Short- and Long-Distance Communication

Waldenmaier¹,

Seibold²,

Seufferlein³

et al. 2021

Cancers

View full text Add to dashboard Cite

Even with all recent advances in cancer therapy, pancreatic cancer still has a dismal 5-year survival rate of less than 7%. The most prevalent tumor subtype is pancreatic ductal adenocarcinoma (PDAC). PDACs display an extensive crosstalk with their tumor microenvironment (TME), e.g., pancreatic stellate cells, but also immune cells to regulate tumor growth, immune evasion, and metastasis. In addition to crosstalk in the local TME, PDACs were shown to induce the formation of pre-metastatic niches in different organs. Recent advances have attributed many of these interactions to intercellular communication by small extracellular vesicles (sEVs, exosomes). These nanovesicles are derived of endo-lysosomal structures (multivesicular bodies) with a size range of 30–150 nm. sEVs carry various bioactive cargos, such as proteins, lipids, DNA, mRNA, or miRNAs and act in an autocrine or paracrine fashion to educate recipient cells. In addition to tumor formation, progression, and metastasis, sEVs were described as potent biomarker platforms for diagnosis and prognosis of PDAC. Advances in sEV engineering have further indicated that sEVs might once be used as effective drug carriers. Thus, extensive sEV-based communication and applications as platform for biomarker analysis or vehicles for treatment suggest a major impact of sEVs in future PDAC research.

show abstract

Recruitment and Expansion of Tregs Cells in the Tumor Environment—How to Target Them?

Cited by 53 publications

References 394 publications

Regulation of T Cells in Cancer by Nitric Oxide

Regulation of T Cells in Cancer by Nitric Oxide

Multifaceted Roles of Chemokines and Chemokine Receptors in Tumor Immunity

Pancreatic Cancer Small Extracellular Vesicles (Exosomes): A Tale of Short- and Long-Distance Communication

Contact Info

Product

Resources

About