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5th Anniversary of 2018 Nobel Prize in Physiology or Medicine:...
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5th Anniversary of 2018 Nobel Prize in Physiology or Medicine: Cancer Immunotherapy

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (15 May 2023) | Viewed by 6143

Special Issue Editors

Dr. Hong-Sook Kim

E-Mail Website
Guest Editor
Department of Biological Sciences, Sungkyunkwan University, Seoul, Korea
Interests: cancer biology; developmental biology; epigenetics; genomics; precision medicine; gene regulation
Dr. Sangeetha Reddy

E-Mail Website
Guest Editor
Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390, USA
Interests: immunotherapy; breast cancer; tumor immunology; antigen presentation; cancer immunology; translational research

Special Issue Information

Dear Colleagues,

The 2018 Nobel Prize in Physiology or Medicine was awarded to James P. Allison and Tasuku Honjo for their discovery of cancer therapy by inhibition of negative immune regulation. In 1996, James P. Allison discovered that blockade of a cell surface molecule on T cells, an immune checkpoint CTLA-4, potentiates effective immune responses against tumor cells. Tasuku Honjo identified and cloned another immune checkpoint, PD-1, in 1992. In early 2000, he discovered different types of T-cell-driven autoimmune syndromes in PD-1 knock-out mice and concluded that PD-1, similar to CTLA-4, acts by negatively controlling immune responses.

The discoveries of these two scientists enabled a deeper understanding of this process and suggested a novel principle for tumor therapy based on removal of the brakes in T cells. Anti-CTLA-4 and anti-PD-1 immune checkpoint inhibitor (ICI) antibodies were developed, and several clinical trials using anti-CTLA-4 antibodies and anti-PD-1 antibodies were successfully carried out with improved clinical outcome in several cancer types, leading to their approval by the US Food and Drug Administration and European Medicines Agency in 2011 and 2015, respectively.

The history of ICIs in cancer treatment is relatively short, but ICI cancer immunotherapy has revolutionized cancer care and led to durable treatment responses in aggressive tumors with otherwise poor outcomes. Unfortunately, only a subset of patient tumors respond to ICIs due to defects in other features of the cancer immunity cycle. Ongoing investigation is underway into stimulating other aspects of anti-tumor immunity to develop novel immunotherapies and combinations with PD-1 and CTLA-4 ICIs. This includes novel immune checkpoints, stimulators of innate immunity, and cellular therapies.  

This Special Issue of Cells aims to collect submissions in the field of cancer immunotherapy with a focus on strategies to enhance the function of immune cells critical for anti-tumor immunity. 

Dr. Hong-Sook Kim
Dr. Sangeetha Reddy
Guest Editors

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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • cancer immunotherapy
  • anti-tumor immunity
  • immunology
  • PD-1
  • CTLA-4
  • immune checkpoint inhibitors

Published Papers (3 papers)

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Research

18 pages, 3608 KiB  
Article
Oxidized Proteins Differentially Affect Maturation and Activation of Human Monocyte-Derived Cells
by Ramona Clemen, Kevin Arlt, Lea Miebach, Thomas von Woedtke and Sander Bekeschus
Cells 2022, 11(22), 3659; https://doi.org/10.3390/cells11223659 - 18 Nov 2022
Cited by 6 | Viewed by 1547
Abstract
In cancer, antigen-presenting cells (APC), including dendritic cells (DCs), take up and process proteins to mount adaptive antitumor immune responses. This often happens in the context of inflamed cancer, where reactive oxygen species (ROS) are ubiquitous to modify proteins. However, the inflammatory consequences [...] Read more.
In cancer, antigen-presenting cells (APC), including dendritic cells (DCs), take up and process proteins to mount adaptive antitumor immune responses. This often happens in the context of inflamed cancer, where reactive oxygen species (ROS) are ubiquitous to modify proteins. However, the inflammatory consequences of oxidized protein uptake in DCs are understudied. To this end, we investigated human monocyte-derived cell surface marker expression and cytokine release profiles when exposed to oxidized and native proteins. Seventeen proteins were analyzed, including viral proteins (e.g., CMV and HBV), inflammation-related proteins (e.g., HO1 and HMGB1), matrix proteins (e.g., Vim and Coll), and vastly in the laboratory used proteins (e.g., BSA and Ova). The multifaceted nature of inflammation-associated ROS was mimicked using gas plasma technology, generating reactive species cocktails for protein oxidation. Fourteen oxidized proteins led to elevated surface marker expression levels of CD25, CD40, CD80, CD86, and MHC-II as well as strongly modified release of IL6, IL8, IL10, IL12, IL23, MCP-1, and TNFα compared to their native counterparts. Especially IL8, heme oxygenase 2, and vimentin oxidation gave pronounced effects. Furthermore, protein kinase phospho-array studies in monocyte-derived cells pulsed with native vs. oxidized IL8 and insulin showed enhanced AKT and RSK2 phosphorylation. In summary, our data provide for the first time an overview of the functional consequences of oxidized protein uptake by human monocyte-derived cells and could therefore be a starting point for exploiting such principle in anticancer therapy in the future. Full article
(This article belongs to the Special Issue 5th Anniversary of 2018 Nobel Prize in Physiology or Medicine: Cancer Immunotherapy)
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21 pages, 2029 KiB  
Article
Preclinical Study of Plasmodium Immunotherapy Combined with Radiotherapy for Solid Tumors
by Zhu Tao, Wenting Ding, Zhipeng Cheng, Yinfang Feng, Zhongkui Kang, Runmin Qiu, Siting Zhao, Wen Hu, Fang Zhou, Donghai Wu, Ziyuan Duan, Li Qin and Xiaoping Chen
Cells 2022, 11(22), 3600; https://doi.org/10.3390/cells11223600 - 14 Nov 2022
Cited by 1 | Viewed by 1890
Abstract
Immune checkpoint blockade therapy (ICB) is ineffective against cold tumors and, although it is effective against some hot tumors, drug resistance can occur. We have developed a Plasmodium immunotherapy (PI) that can overcome these shortcomings. However, the specific killing effect of PI on [...] Read more.
Immune checkpoint blockade therapy (ICB) is ineffective against cold tumors and, although it is effective against some hot tumors, drug resistance can occur. We have developed a Plasmodium immunotherapy (PI) that can overcome these shortcomings. However, the specific killing effect of PI on tumor cells is relatively weak. Radiotherapy (RT) is known to have strong specific lethality to tumor cells. Therefore, we hypothesized that PI combined with RT could produce synergistic antitumor effects. We tested our hypothesis using orthotopic and subcutaneous models of mouse glioma (GL261, a cold tumor) and a subcutaneous model of mouse non-small cell lung cancer (NSCLC, LLC, a hot tumor). Our results showed that, compared with each monotherapy, the combination therapy more significantly inhibited tumor growth and extended the life span of tumor-bearing mice. More importantly, the combination therapy could cure approximately 70 percent of glioma. By analyzing the immune profile of the tumor tissues, we found that the combination therapy was more effective in upregulating the perforin-expressing effector CD8+ T cells and downregulating the myeloid-derived suppressor cells (MDSCs), and was thus more effective in the treatment of cancer. The clinical transformation of PI combined with RT in the treatment of solid tumors, especially glioma, is worthy of expectation. Full article
(This article belongs to the Special Issue 5th Anniversary of 2018 Nobel Prize in Physiology or Medicine: Cancer Immunotherapy)
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18 pages, 3775 KiB  
Article
A Novel P53 Nanomedicine Reduces Immunosuppression and Augments Anti-PD-1 Therapy for Non-Small Cell Lung Cancer in Syngeneic Mouse Models
by Sang-Soo Kim, Joe B. Harford, Manish Moghe, Caroline Doherty and Esther H. Chang
Cells 2022, 11(21), 3434; https://doi.org/10.3390/cells11213434 - 31 Oct 2022
Cited by 5 | Viewed by 2268
Abstract
Lung cancer is among the most common and lethal cancers and warrants novel therapeutic approaches to improving patient outcomes. Although immune checkpoint inhibitors (ICIs) have demonstrated substantial clinical benefits, most patients remain unresponsive to currently approved ICIs or develop resistance after initial response. [...] Read more.
Lung cancer is among the most common and lethal cancers and warrants novel therapeutic approaches to improving patient outcomes. Although immune checkpoint inhibitors (ICIs) have demonstrated substantial clinical benefits, most patients remain unresponsive to currently approved ICIs or develop resistance after initial response. Many ongoing clinical studies are investigating combination therapies to address the limited efficacy of ICIs. Here, we have assessed whether p53 gene therapy via a tumor-targeting nanomedicine (termed SGT-53) can augment anti-programmed cell death-1 (PD-1) immunotherapy to expand its use in non-responding patients. Using syngeneic mouse models of lung cancers that are resistant to anti-PD-1, we demonstrate that restoration of normal p53 function potentiates anti-PD-1 to inhibit tumor growth and prolong survival of tumor-bearing animals. Our data indicate that SGT-53 can restore effective immune responses against lung cancer cells by reducing immuno-suppressive cells (M2 macrophages and regulatory T cells) and by downregulating immunosuppressive molecules (e.g., galectin-1, a negative regulator of T cell activation and survival) while increasing activity of cytotoxic T cells. These results suggest that combining SGT-53 with anti-PD-1 immunotherapy could increase the fraction of lung cancer patients that responds to anti-PD-1 therapy and support evaluation of this combination particularly in patients with ICI-resistant lung cancers. Full article
(This article belongs to the Special Issue 5th Anniversary of 2018 Nobel Prize in Physiology or Medicine: Cancer Immunotherapy)
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