Landscape of Myeloid-derived Suppressor Cell in Tumor Immunotherapy

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Abstract

Myeloid-derived suppressor cells (MDSC) are a group of immature cells that produced by emergency myelopoiesis. Emerging evidences have identified the vital role of MDSC in cancer microenvironment, in which MDSC exerts both immunological and non-immunological activities to assist the progression of cancer. Advances in pre-clinical research have provided us the understanding of MDSC in cancer context from the perspective of molecular mechanism. In clinical scenario, MDSC and its subsets have been discovered to exist in peripheral blood and tumor site of patients from various types of cancers. In this review, we highlight the clinical value of MDSC in predicting prognosis of cancer patients and the responses of immunotherapies, therefore to propose the MDSC-inhibiting strategy in the scenario of cancer immunotherapies. Phenotypes and biological functions of MDSC in cancer microenvironment are comprehensively summarized to provide potential targets of MDSC-inhibiting strategy from the aspect of molecular mechanisms.

Supplementary Information

The online version contains supplementary material available at 10.1186/s40364-021-00333-5.

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Most cited references 193

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Improved Survival with Ipilimumab in Patients with Metastatic Melanoma

F. Stephen Hodi, Steven J O'Day, David F McDermott … (2010)

An improvement in overall survival among patients with metastatic melanoma has been an elusive goal. In this phase 3 study, ipilimumab--which blocks cytotoxic T-lymphocyte-associated antigen 4 to potentiate an antitumor T-cell response--administered with or without a glycoprotein 100 (gp100) peptide vaccine was compared with gp100 alone in patients with previously treated metastatic melanoma. A total of 676 HLA-A*0201-positive patients with unresectable stage III or IV melanoma, whose disease had progressed while they were receiving therapy for metastatic disease, were randomly assigned, in a 3:1:1 ratio, to receive ipilimumab plus gp100 (403 patients), ipilimumab alone (137), or gp100 alone (136). Ipilimumab, at a dose of 3 mg per kilogram of body weight, was administered with or without gp100 every 3 weeks for up to four treatments (induction). Eligible patients could receive reinduction therapy. The primary end point was overall survival. The median overall survival was 10.0 months among patients receiving ipilimumab plus gp100, as compared with 6.4 months among patients receiving gp100 alone (hazard ratio for death, 0.68; P<0.001). The median overall survival with ipilimumab alone was 10.1 months (hazard ratio for death in the comparison with gp100 alone, 0.66; P=0.003). No difference in overall survival was detected between the ipilimumab groups (hazard ratio with ipilimumab plus gp100, 1.04; P=0.76). Grade 3 or 4 immune-related adverse events occurred in 10 to 15% of patients treated with ipilimumab and in 3% treated with gp100 alone. There were 14 deaths related to the study drugs (2.1%), and 7 were associated with immune-related adverse events. Ipilimumab, with or without a gp100 peptide vaccine, as compared with gp100 alone, improved overall survival in patients with previously treated metastatic melanoma. Adverse events can be severe, long-lasting, or both, but most are reversible with appropriate treatment. (Funded by Medarex and Bristol-Myers Squibb; ClinicalTrials.gov number, NCT00094653.)

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Safety and Activity of Anti–PD-L1 Antibody in Patients with Advanced Cancer

Julie Brahmer, Scott Tykodi, Laura Q.M. Chow … (2012)

Programmed death 1 (PD-1) protein, a T-cell coinhibitory receptor, and one of its ligands, PD-L1, play a pivotal role in the ability of tumor cells to evade the host's immune system. Blockade of interactions between PD-1 and PD-L1 enhances immune function in vitro and mediates antitumor activity in preclinical models. In this multicenter phase 1 trial, we administered intravenous anti-PD-L1 antibody (at escalating doses ranging from 0.3 to 10 mg per kilogram of body weight) to patients with selected advanced cancers. Anti-PD-L1 antibody was administered every 14 days in 6-week cycles for up to 16 cycles or until the patient had a complete response or confirmed disease progression. As of February 24, 2012, a total of 207 patients--75 with non-small-cell lung cancer, 55 with melanoma, 18 with colorectal cancer, 17 with renal-cell cancer, 17 with ovarian cancer, 14 with pancreatic cancer, 7 with gastric cancer, and 4 with breast cancer--had received anti-PD-L1 antibody. The median duration of therapy was 12 weeks (range, 2 to 111). Grade 3 or 4 toxic effects that investigators considered to be related to treatment occurred in 9% of patients. Among patients with a response that could be evaluated, an objective response (a complete or partial response) was observed in 9 of 52 patients with melanoma, 2 of 17 with renal-cell cancer, 5 of 49 with non-small-cell lung cancer, and 1 of 17 with ovarian cancer. Responses lasted for 1 year or more in 8 of 16 patients with at least 1 year of follow-up. Antibody-mediated blockade of PD-L1 induced durable tumor regression (objective response rate of 6 to 17%) and prolonged stabilization of disease (rates of 12 to 41% at 24 weeks) in patients with advanced cancers, including non-small-cell lung cancer, melanoma, and renal-cell cancer. (Funded by Bristol-Myers Squibb and others; ClinicalTrials.gov number, NCT00729664.).

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Accessories to the crime: functions of cells recruited to the tumor microenvironment.

Douglas Hanahan, Lisa M. Coussens (2012)

Mutationally corrupted cancer (stem) cells are the driving force of tumor development and progression. Yet, these transformed cells cannot do it alone. Assemblages of ostensibly normal tissue and bone marrow-derived (stromal) cells are recruited to constitute tumorigenic microenvironments. Most of the hallmarks of cancer are enabled and sustained to varying degrees through contributions from repertoires of stromal cell types and distinctive subcell types. Their contributory functions to hallmark capabilities are increasingly well understood, as are the reciprocal communications with neoplastic cancer cells that mediate their recruitment, activation, programming, and persistence. This enhanced understanding presents interesting new targets for anticancer therapy. Copyright Â© 2012 Elsevier Inc. All rights reserved.

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Author and article information

Contributors

Zhenya Hong: hongzhenya@126.com

Zhiqiang Han: hanzq2003@126.com

Journal

Journal ID (nlm-ta): Biomark Res

Journal ID (iso-abbrev): Biomark Res

Title: Biomarker Research

Publisher: BioMed Central (London )

ISSN (Electronic): 2050-7771

Publication date (Electronic): 24 October 2021

Publication date PMC-release: 24 October 2021

Publication date Collection: 2021

Volume: 9

Electronic Location Identifier: 77

Affiliations

[1 ]GRID grid.24696.3f, ISNI 0000 0004 0369 153X, Department of Neurosurgery, Beijing TianTan Hospital, , Capital Medical University, ; Beijing, China

[2 ]GRID grid.33199.31, ISNI 0000 0004 0368 7223, Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, , Huazhong University of Science and Technology, ; Wuhan, 430030 Hubei China

[3 ]GRID grid.506261.6, ISNI 0000 0001 0706 7839, Department of Gynecology and Oncology, National Cancer Center/Cancer Hospital, , Chinese Academy of Medical Sciences and Peking Union Medical College, ; Beijing, China

[4 ]GRID grid.33199.31, ISNI 0000 0004 0368 7223, Department of Hematology, Tongji Hospital, Tongji Medical College, , Huazhong University of Science and Technology, ; Wuhan, 430030 Hubei China

Article

Publisher ID: 333

DOI: 10.1186/s40364-021-00333-5

PMC ID: 8543853

PubMed ID: 34689842

SO-VID: edbdff44-ca5a-43d7-9290-4915ed3b5a75

License:

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

History

Date received : 17 August 2021

Date accepted : 26 September 2021

Funding

Funded by: FundRef http://dx.doi.org/10.13039/501100001809, national natural science foundation of china;

Award ID: 81974414

Award ID: 81772788

Award ID: 81873430

Award Recipient : Zhenya Hong Zhiqiang Han

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Keywords: myeloid-derived suppressor cells,tumor,immunotherapy

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Keywords: myeloid-derived suppressor cells, tumor, immunotherapy

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Landscape of Myeloid-derived Suppressor Cell in Tumor Immunotherapy

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Supplementary Information

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Cancer Immunotherapy

Most cited references 193

Improved Survival with Ipilimumab in Patients with Metastatic Melanoma

Safety and Activity of Anti–PD-L1 Antibody in Patients with Advanced Cancer

Accessories to the crime: functions of cells recruited to the tumor microenvironment.

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Cited by 34

Most referenced authors 3,611