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Cancer-Induced Immunosuppressive Mechanism
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Cancer-Induced Immunosuppressive Mechanism

A special issue of Journal of Personalized Medicine (ISSN 2075-4426). This special issue belongs to the section "Mechanisms of Diseases".

Deadline for manuscript submissions: closed (25 March 2022) | Viewed by 14468

Special Issue Editor

Dr. Malgorzata Czystowska-Kuzmicz

E-Mail Website
Guest Editor
Chair and Department of Biochemistry, Medical University of Warsaw, 00-927 Warszawa, Poland
Interests: immuno-oncology; tumor-derived extracellular vesicles; tumor microenvironment; cancer immunotherapy; immune suppression in cancer and its mechanisms; exosomes in pathological conditions

Special Issue Information

Dear Colleagues,

The development of immune-based therapies in the last decade, including monoclonal antibodies; adoptive cell transfer; vaccines; and, especially, immune-checkpoint inhibitors, has produced tremendous success in the treatment of some types of cancer and raised expectations for immunotherapy as the ultimate cure for cancer. However, low response rates and the frequent lack of long-term benefits in patients have called scientists’ and clinicians’ attention to the complex crosstalk between tumor and immune cells. Indeed, it has become increasingly clear that tumors use several mechanisms to suppress anti-tumor immunity, within the tumor microenvironment as well as systemically, and that this escape of tumors from the host immune system may be a major barrier to successful immunotherapy. Therefore, the identification and understanding of the various tumor-induced immunosuppressive mechanisms is essential for the future development of effective immunotherapies and may provide new therapeutic targets. This Special Issue will bring together the newest original research, short communications, and review articles on tumor-induced immune suppression, including such topics as immunosuppressive factors, recruitment of suppressive or regulatory cells, immune cell reprogramming, tumor microenviroment editing, immune checkpoints, the role of EVs in cancer/immune cell cross-talk , metabolics, and tumor-derived EVs.

Dr. Malgorzata Czystowska-Kuzmicz
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Personalized Medicine is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • tumor-induced immunosuppressive mechanisms
  • cancer immuno-editing
  • tumor microenviroment
  • cellular cross-talk
  • immune checkpoints
  • tumor biomarker
  • metabolic reprogramming
  • immunotherapy
  • T-cell exhaustion
  • tumor extracellular vesicles

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Published Papers (4 papers)

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Research

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14 pages, 2481 KiB  
Article
Breast Cancer Cell-Derived Adenosine Enhances Generation and Suppressor Function of Human Adaptive Regulatory T Cells
by Magis Mandapathil, Miroslaw J. Szczepanski, Edwin K. Jackson, Stephan Lang and Theresa L. Whiteside
J. Pers. Med. 2021, 11(8), 754; https://doi.org/10.3390/jpm11080754 - 30 Jul 2021
Cited by 3 | Viewed by 2552
Abstract
Introduction: Adaptive regulatory T cells (Tr1) are induced in the periphery by environmental stimuli. CD73 expression and adenosine (ADO) production by tumor cells may influence Tr1 generation and their immunosuppressive activity. Material and Methods: Tr1 were generated in co-cultures of CD4+CD25neg T cells, [...] Read more.
Introduction: Adaptive regulatory T cells (Tr1) are induced in the periphery by environmental stimuli. CD73 expression and adenosine (ADO) production by tumor cells may influence Tr1 generation and their immunosuppressive activity. Material and Methods: Tr1 were generated in co-cultures of CD4+CD25neg T cells, autologous immature dendritic cells (iDC), and irradiated ADO-producing CD73+ or non-producing CD73neg breast cancer (BrCa) cell lines (TU). The expression of ectonucleotidases and other surface markers on Tr1 was determined by flow cytometry. Tr1-mediated suppression of proliferation was evaluated in CFSE-based assays. Luciferase-based ATP detection assays and mass spectrometry were used to measure ATP hydrolysis and ADO levels. Cytokine levels were measured by ELISA or Luminex. CD73 expression on tumor cells or T cells in TU tissues was assessed by immunofluorescence. Results: CD73+ TU induced higher numbers of Tr1 cells (p < 0.01) than CD73neg TU. Tr1TU73+ hydrolyzed more exogenous ATP, produced more ADO, and mediated higher suppression than Tr1TU73neg (p < 0.05 for all). ARL67156, an ectonucleotidase inhibitor, and ZM241385, A2A receptor antagonist, reduced suppression of proliferation mediated by Tr1TU73+ cells (p < 0.01). Basal-like primary BrCa cells expressed higher levels of ectonucleotidases and induced more Tr1 than less aggressive primary luminal-like BrCa. Conclusion: BrCa producing ADO (CD73+ TU) favor the induction of Tr1, which expresses CD39 and CD73, hydrolyzes ATP to ADO, and effectively suppresses anti-tumor immunity. Full article
(This article belongs to the Special Issue Cancer-Induced Immunosuppressive Mechanism)
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21 pages, 6298 KiB  
Article
A Proteomic Atlas of Lineage and Cancer-Polarized Expression Modules in Myeloid Cells Modeling Immunosuppressive Tumor-Infiltrating Subsets
by Ester Blanco, Maria Ibañez-Vea, Carlos Hernandez, Lylia Drici, Xabier Martínez de Morentin, Maria Gato, Karina Ausin, Ana Bocanegra, Miren Zuazo, Luisa Chocarro, Hugo Arasanz, Gonzalo Fernandez-Hinojal, Joaquin Fernandez-Irigoyen, Cristian Smerdou, Maider Garnica, Miriam Echaide, Leticia Fernandez, Pilar Morente, Pablo Ramos-Castellanos, Diana Llopiz, Enrique Santamaria, Martin R. Larsen, David Escors and Grazyna Kochanadd Show full author list remove Hide full author list
J. Pers. Med. 2021, 11(6), 542; https://doi.org/10.3390/jpm11060542 - 11 Jun 2021
Cited by 6 | Viewed by 3910
Abstract
Monocytic and granulocytic myeloid-derived suppressor cells together with tumor-infiltrating macrophages constitute the main tumor-infiltrating immunosuppressive myeloid populations. Due to the phenotypic resemblance to conventional myeloid cells, their identification and purification from within the tumors is technically difficult and makes their study a challenge. [...] Read more.
Monocytic and granulocytic myeloid-derived suppressor cells together with tumor-infiltrating macrophages constitute the main tumor-infiltrating immunosuppressive myeloid populations. Due to the phenotypic resemblance to conventional myeloid cells, their identification and purification from within the tumors is technically difficult and makes their study a challenge. We differentiated myeloid cells modeling the three main tumor-infiltrating types together with uncommitted macrophages, using ex vivo differentiation methods resembling the tumor microenvironment. The phenotype and proteome of these cells was compared to identify linage-dependent relationships and cancer-specific interactome expression modules. The relationships between monocytic MDSCs and TAMs, monocytic MDSCs and granulocytic MDSCs, and hierarchical relationships of expression networks and transcription factors due to lineage and cancer polarization were mapped. Highly purified immunosuppressive myeloid cell populations that model tumor-infiltrating counterparts were systematically analyzed by quantitative proteomics. Full functional interactome maps have been generated to characterize at high resolution the relationships between the three main myeloid tumor-infiltrating cell types. Our data highlights the biological processes related to each cell type, and uncover novel shared and differential molecular targets. Moreover, the high numbers and fidelity of ex vivo-generated subsets to their natural tumor-shaped counterparts enable their use for validation of new treatments in high-throughput experiments. Full article
(This article belongs to the Special Issue Cancer-Induced Immunosuppressive Mechanism)
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Review

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18 pages, 1112 KiB  
Review
Extracellular Vesicles—A New Potential Player in the Immunology of Renal Cell Carcinoma
by Marcin Kleibert, Miłosz Majka, Klaudia Łakomska and Małgorzata Czystowska-Kuźmicz
J. Pers. Med. 2022, 12(5), 772; https://doi.org/10.3390/jpm12050772 - 10 May 2022
Cited by 4 | Viewed by 3924
Abstract
The incidence of renal cell carcinoma (RCC) has doubled in the developed world within the last fifty years, and now it is responsible for 2–3% of diagnosed cancers. The delay in diagnosis and the not fully understood pathogenesis are the main challenges that [...] Read more.
The incidence of renal cell carcinoma (RCC) has doubled in the developed world within the last fifty years, and now it is responsible for 2–3% of diagnosed cancers. The delay in diagnosis and the not fully understood pathogenesis are the main challenges that have to be overcome. It seems that extracellular vesicles (EVs) are one of the key players in tumor development since they ensure a proper microenvironment for the tumor cells. The stimulation of angiogenesis and immunosuppression is mediated by molecules contained in EVs. It was shown that EVs derived from cancer cells can inhibit T cell proliferation, natural killer lymphocyte activation, and dendritic cell maturation by this mechanism. Moreover, EVs may be a biomarker for the response to anti-cancer treatment. In this review, we sum up the knowledge about the role of EVs in RCC pathogenesis and show their future perspectives in this field. Full article
(This article belongs to the Special Issue Cancer-Induced Immunosuppressive Mechanism)
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22 pages, 1500 KiB  
Review
Liquid Biopsy Biomarkers for Immunotherapy in Non-Small Cell Lung Carcinoma: Lessons Learned and the Road Ahead
by Jesus Hita-Millan, Angel Carracedo and Ceres Fernandez-Rozadilla
J. Pers. Med. 2021, 11(10), 971; https://doi.org/10.3390/jpm11100971 - 28 Sep 2021
Cited by 5 | Viewed by 2995
Abstract
Over the recent years, advances in the development of anti-cancer treatments, particularly the implementation of ICIs (immune checkpoint inhibitors), have resulted in increased survival rates in NSCLC (non-small cell lung cancer) patients. However, a significant proportion of patients does not seem respond to [...] Read more.
Over the recent years, advances in the development of anti-cancer treatments, particularly the implementation of ICIs (immune checkpoint inhibitors), have resulted in increased survival rates in NSCLC (non-small cell lung cancer) patients. However, a significant proportion of patients does not seem respond to immunotherapy, and some individuals even develop secondary resistance to treatment. Therefore, it is imperative to correctly identify the patients that will benefit from ICI therapy in order to tailor therapeutic options in an individualised setting, ultimately benefitting both the patient and the health system. Many different biomarkers have been explored to correctly stratify patients and predict response to immunotherapy, but liquid biopsy approaches have recently arisen as an interesting opportunity to predict and monitor treatment response due to their logistic accessibility. This review summarises the current data and efforts in the field of ICI response biomarkers in NSCLC patients and highlights advantages and limitations as we discuss the road to clinical implementation. Full article
(This article belongs to the Special Issue Cancer-Induced Immunosuppressive Mechanism)
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