Abstract 2876: Inflammation of the tumor microenvironment is regulated by myeloid derived suppressor cell and macrophage crosstalk.

2013 ◽  
Author(s):  
Daniel W. Beury ◽  
Katherine H. Parker ◽  
Suzanne Ostrand-Rosenberg
Keyword(s):  
Tumor Microenvironment ◽  
Suppressor Cell ◽  
Myeloid Derived Suppressor Cell

Metabolic changes and interaction of tumor cell, myeloid-derived suppressor cell and T cell in hypoxic microenvironment

2020 ◽  
Author(s):  
Xiantu Ou ◽  
Weibiao Lv
Keyword(s):  
Tumor Microenvironment ◽  
Regulatory Protein ◽  
Tumor Hypoxia ◽  
Suppressor Cells ◽  
Suppressor Cell ◽  
Inflammatory Factors ◽  
Tumor Escape ◽  
Myeloid Derived Suppressor Cells ◽  
Myeloid Derived Suppressor Cell ◽  
Transcriptional Regulatory

It is universally acknowledged that a large number of immune cells, as well as inflammatory factors, regulatory factors and metabolites, accumulate in the tumor microenvironment to jointly promote tumor escape, development and metastasis. Hypoxia is one of the characteristics in tumor microenvironment and is a common phenomenon in all solid tumors. In tumor hypoxia response, there is a key regulator called HIF-1a, which is a key transcriptional regulatory protein that regulates many critical genes. In this paper, the effects of hypoxia on glucose metabolism of tumor cells, myeloid-derived suppressor cells and T cells in tumor microenvironment were reviewed, and the interaction among the three was also described.

ARGX-111 shows activity in MET-amplified patients in a phase-I study and in preclinical models of myeloid-derived suppressor cell (MDSC) depletion in the tumor microenvironment.

2016 ◽  
Vol 34 (15_suppl) ◽  
pp. e14016-e14016 ◽  
Author(s):  
Christian Diego Rolfo ◽  
Philippe Georges Aftimos ◽  
Jean-Rene Pallandre ◽  
Virginia Morello ◽  
Adeline Bouard ◽  
...  
Keyword(s):  
Tumor Microenvironment ◽  
Phase I ◽  
Phase I Study ◽  
Suppressor Cell ◽  
Preclinical Models ◽  
Myeloid Derived Suppressor Cell

scholarly journals STING signaling remodels the tumor microenvironment by antagonizing myeloid-derived suppressor cell expansion

2019 ◽  
Vol 26 (11) ◽  
pp. 2314-2328 ◽  
Author(s):  
Chuan-xia Zhang ◽  
Shu-biao Ye ◽  
Jian-jiao Ni ◽  
Ting-ting Cai ◽  
Yi-na Liu ◽  
...  
Keyword(s):  
Tumor Microenvironment ◽  
Cell Expansion ◽  
Suppressor Cell ◽  
Myeloid Derived Suppressor Cell

scholarly journals TLR9 ligation in pancreatic stellate cells promotes tumorigenesis

2015 ◽  
Vol 212 (12) ◽  
pp. 2077-2094 ◽  
Author(s):  
Constantinos P. Zambirinis ◽  
Elliot Levie ◽  
Susanna Nguy ◽  
Antonina Avanzi ◽  
Rocky Barilla ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Microenvironment ◽  
Pancreatic Carcinoma ◽  
Suppressor Cell ◽  
Stellate Cells ◽  
Pancreatic Stellate Cells ◽  
Cell Recruitment ◽  
Myeloid Derived Suppressor Cell ◽  
Epithelial Compartment ◽  
Tlr9 Activation

Modulation of Toll-like receptor (TLR) signaling can have protective or protumorigenic effects on oncogenesis depending on the cancer subtype and on specific inflammatory elements within the tumor milieu. We found that TLR9 is widely expressed early during the course of pancreatic transformation and that TLR9 ligands are ubiquitous within the tumor microenvironment. TLR9 ligation markedly accelerates oncogenesis, whereas TLR9 deletion is protective. We show that TLR9 activation has distinct effects on the epithelial, inflammatory, and fibrogenic cellular subsets in pancreatic carcinoma and plays a central role in cross talk between these compartments. Specifically, TLR9 activation can induce proinflammatory signaling in transformed epithelial cells, but does not elicit oncogene expression or cancer cell proliferation. Conversely, TLR9 ligation induces pancreatic stellate cells (PSCs) to become fibrogenic and secrete chemokines that promote epithelial cell proliferation. TLR9-activated PSCs mediate their protumorigenic effects on the epithelial compartment via CCL11. Additionally, TLR9 has immune-suppressive effects in the tumor microenvironment (TME) via induction of regulatory T cell recruitment and myeloid-derived suppressor cell proliferation. Collectively, our work shows that TLR9 has protumorigenic effects in pancreatic carcinoma which are distinct from its influence in extrapancreatic malignancies and from the mechanistic effects of other TLRs on pancreatic oncogenesis.

scholarly journals Distinct cell adhesion signature defines glioblastoma myeloid-derived suppressor cell subsets

2021 ◽  
Author(s):  
Defne Bayik ◽  
Cynthia F. Bartels ◽  
Katreya Lovrenert ◽  
Dionysios Watson ◽  
Duo Zhang ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Tumor Microenvironment ◽  
Immune Suppression ◽  
Molecular Basis ◽  
Therapeutic Response ◽  
Myeloid Cell ◽  
Suppressor Cell ◽  
Myeloid Derived Suppressor Cell ◽  
Distinct Cell ◽  
Immunotherapy Target

Increased myeloid-derived suppressor cell (MDSC) frequency is associated with worse outcomes and poor therapeutic response in glioblastoma (GBM). Monocytic (m) MDSCs represent the predominant subset in the GBM microenvironment. However, the molecular basis of mMDSC enrichment in the tumor microenvironment compared to granulocytic (g) MDSCs has yet to be determined. Here, we report that mMDSCs and gMDSCs display differences in their tumor-accelerating ability, with mMDSCs driving tumor growth in GBM models. Epigenetic assessments indicate enhanced gene accessibility for cell adhesion programs in mMDSCs and higher cell-surface integrin expression in mouse and human mMDSCs. Integrin b1 blockage abrogated the tumor-promoting phenotype of mMDSCs and altered the immune profile in the tumor microenvironment. These findings suggest that integrin b1 expression underlies the enrichment of mMDSCs in tumors and represents a putative immunotherapy target to attenuate myeloid cell-driven immune suppression in GBM.

scholarly journals Ablative Radiotherapy Reprograms the Tumor Microenvironment of a Pancreatic Tumor in Favoring the Immune Checkpoint Blockade Therapy

2021 ◽  
Vol 22 (4) ◽  
pp. 2091
Author(s):  
Yu-Hung Lee ◽  
Ching-Fang Yu ◽  
Ying-Chieh Yang ◽  
Ji-Hong Hong ◽  
Chi-Shiun Chiang
Keyword(s):  
Pancreatic Cancer ◽  
Tumor Microenvironment ◽  
Immune Checkpoint ◽  
Pancreatic Tumor ◽  
Tumor Model ◽  
Suppressor Cell ◽  
Immune Checkpoint Blockade ◽  
Checkpoint Blockade ◽  
Control Group ◽  
Myeloid Derived Suppressor Cell

The low overall survival rate of patients with pancreatic cancer has driven research to seek a new therapeutic protocol. Radiotherapy (RT) is frequently an option in the neoadjuvant or palliative settings for pancreatic cancer treatment. This study explored the effect of RT protocols on the tumor microenvironment (TME) and their consequent impact on anti-programmed cell death ligand-1 (PD-L1) therapy. Using a murine orthotopic pancreatic tumor model, UN-KC-6141, RT-disturbed TME was examined by immunohistochemical staining. The results showed that ablative RT is more effective than fractionated RT at recruiting T cells. On the other hand, fractionated RT induces more myeloid-derived suppressor cell infiltration than ablative RT. The RT-disturbed TME presents a higher perfusion rate per vessel. The increase in vessel perfusion is associated with a higher amount of anti-PD-L1 antibody being delivered to the tumor. Animal survival is increased by anti-PD-L1 therapy after ablative RT, with 67% of treated animals surviving more than 30 days after tumor inoculation compared to a median survival time of 16.5 days for the control group. Splenocytes isolated from surviving animals were specifically cytotoxic for UN-KC-6141 cells. We conclude that the ablative RT-induced TME is more suited than conventional RT-induced TME to combination therapy with immune checkpoint blockade.

scholarly journals Targeting MDSC for Immune-Checkpoint Blockade in Cancer Immunotherapy: Current Progress and New Prospects

2021 ◽  
Vol 15 ◽  
pp. 117955492110355
Author(s):  
Tianhang Li ◽  
Tianyao Liu ◽  
Wenjie Zhu ◽  
Shangxun Xie ◽  
Zihan Zhao ◽  
...  
Keyword(s):  
Immune Checkpoint ◽  
Immune Escape ◽  
Suppressor Cell ◽  
Immune Checkpoint Blockade ◽  
Checkpoint Blockade ◽  
Great Promise ◽  
Therapy Process ◽  
Myeloid Derived Suppressor Cell ◽  
Anti Cancer ◽  
Immune Suppressor

Immune-checkpoint blockade (ICB) demonstrated inspiring effect and great promise in anti-cancer therapy. However, many obstacles, such as drug resistance and difficulty in patient selection, limited the efficacy of ICB therapy and awaited to be overcome. By timely identification and intervention of the key immune-suppressive promotors in the tumor microenvironment (TME), we may better understand the mechanisms of cancer immune-escape and use novel strategies to enhance the therapeutic effect of ICB. Myeloid-derived suppressor cell (MDSC) is recognized as a major immune suppressor in the TME. In this review, we summarized the roles MDSC played in the cancer context, focusing on its negative biologic functions in ICB therapy, discussed the strategies targeted on MDSC to optimize the diagnosis and therapy process of ICB and improve the efficacy of ICB therapy against malignancies.

Sign in / Sign up

Export Citation Format

Share Document