Anti-Tumor Immune Responses 2.0

Topic Information

Dear Colleagues,

It remains unclear how and when, during multi-step tumor progression via clonal selection, cancer cells are selected for their high mutational burden, as well as how the immune system is first alerted to their presence and begins its initial, often unsuccessful, attempts at eliminating them. At present, it is impossible to say which of the dozens of immunotherapy strategies under development will become the precursors of anti-cancer treatments that will prove to be vastly more effective than those developed to date and that will generate robust, durable responses for the majority of patients receiving treatment. For example, advances in molecular genetics, biochemistry, virus biology, cellular and system biology, and cellular immunology have recently converged with discoveries in drugs and antibodies to generate novel, potentially powerful ways to harness the immune response to eradicate human tumors. At this time, the action of the immune system has improved two types of attacks against infectious agents or cells targeted for destruction or neutralization. These involve humoral and cellular immunity, as some types of cells, particularly macrophages and NK cells, have an innate ability to recognize cells that should be destroyed. In this issue, we would like to discuss the frontiers in this area of research concerning cancer cell types where these phenomena have been proven to be positively active at the level of hematopoietic malignancies and, most importantly, in solid tumors with advanced immune therapies. Examples of instances where these strategies fail are of great value for better understanding how cancer cells evade this immune mechanism using the most recent genome biology technologies to determine which other genes/proteins/pathways are involved in these coordinated, interconnecting actions.

Prof. Dr. Massimo Zollo
Dr. Renata Grifantini
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Antibodies antibodies	3.0	7.1	2012	23 Days	CHF 1800
Cancers cancers	4.5	8.0	2009	16.3 Days	CHF 2900
Immuno immuno	2.1	2.6	2021	28.1 Days	CHF 1000
International Journal of Molecular Sciences ijms	4.9	8.1	2000	18.1 Days	CHF 2900
Vaccines vaccines	5.2	8.9	2013	17.6 Days	CHF 2700

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Published Papers (5 papers)

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All Antibodies Cancers Immuno IJMS Vaccines

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17 pages, 897 KiB  

Open AccessArticle

Association of HLA-G Expression, Its Genetic Variants and Related Neuro-Immunomodulation with Characteristics of Bladder Carcinoma

by Vladimira Durmanova, Iveta Mikolaskova, Eszter Zsemlye, Agata Ocenasova, Helena Bandzuchova, Magda Suchankova, Boris Kollarik, Patrik Palacka, Milan Zvarik, Maria Bucova and Luba Hunakova

Cancers 2024, 16(22), 3877; https://doi.org/10.3390/cancers16223877 - 20 Nov 2024

Viewed by 485

Abstract

Background: Human leukocyte antigen G (HLA-G) is an immune checkpoint molecule with immunosuppressive and anti-inflammatory activities. It belongs to class I non-classical major histocompatibility complex molecules and has been upregulated in various cancer types. In bladder cancer (BC) tumors, the association of HLA-G [...] Read more.

Background: Human leukocyte antigen G (HLA-G) is an immune checkpoint molecule with immunosuppressive and anti-inflammatory activities. It belongs to class I non-classical major histocompatibility complex molecules and has been upregulated in various cancer types. In bladder cancer (BC) tumors, the association of HLA-G with cancer progression has to be explained. Methods: A total of 89 BC patients and 74 control subjects were genotyped for the HLA-G 14 bp ins/del polymorphism. In urine cell samples, HLA-G mRNA expression was analyzed using real-time PCR. Soluble HLA-G (sHLA-G) serum levels were measured by ELISA. The associations between the HLA-G 14 bp ins/del polymorphism, HLA-G mRNA expression, and/or sHLA-G levels and selected variables including tumor grade, disease stage, body mass index, and heart rate variability (HRV) parameters were evaluated. Results: The protective HLA-G 14 bp ins/ins genotype under the recessive genetic model was associated with lower HLA-G mRNA expression in the BC group (p = 0.049). Significantly higher HLA-G mRNA expression was detected in patients with pT2 + pT3 as compared to those with pTa + pT1 stages (p = 0.0436). Furthermore, higher HLA-G mRNA expression was observed in high-grade muscle-infiltrating BC (MIBC) than in the low-grade non-MIBC group (p = 0.0365). Patients with a level of sHLA-G above 29 U/mL had shorter disease-free survival than patients with lower sHLA-G levels. Furthermore, the opposite HRV correlations with sHLA-G levels in BC patients as compared to controls probably reflect the different roles of HLA-G in health and cancer. Conclusions: Our results suggest the impact of the HLA-G 14 bp ins/del variant, HLA-G expression, and autonomic nervous system imbalance on advanced stages of BC. Full article

(This article belongs to the Topic Anti-Tumor Immune Responses 2.0)

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13 pages, 1246 KiB  

Open AccessSystematic Review

Combined Radiotherapy and Hyperthermia: A Systematic Review of Immunological Synergies for Amplifying Radiation-Induced Abscopal Effects

by Loïc Van Dieren, Tom Quisenaerts, Mackenzie Licata, Arnaud Beddok, Alexandre G. Lellouch, Dirk Ysebaert, Vera Saldien, Marc Peeters and Ivana Gorbaslieva

Cancers 2024, 16(21), 3656; https://doi.org/10.3390/cancers16213656 - 30 Oct 2024

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Abstract

Introduction: The abscopal effect is a systemic immune response characterized by metastases regression at sites distant from the irradiated lesion. This systematic review aims to explore the immunological mechanisms of action underlying the abscopal effect and to investigate how hyperthermia (HT) can increase [...] Read more.

Introduction: The abscopal effect is a systemic immune response characterized by metastases regression at sites distant from the irradiated lesion. This systematic review aims to explore the immunological mechanisms of action underlying the abscopal effect and to investigate how hyperthermia (HT) can increase the chances of radiotherapy (RT) triggering systemic anti-tumor immune responses. Methods: This review is created in accordance with the PRISMA guidelines. Results and Conclusion: HT and RT have both complementary and synergistic immunological effects. Both methods trigger danger signal release, promoting cytokine and chemokine secretion, which increases T-cell infiltration and facilitates cell death. Both treatments upregulate extracellular tumor HSP70, which could amplify DAMP recognition by macrophages and DCs, leading to stronger tumor antigen presentation and CTL-mediated immune responses. Additionally, the combined increase in cell adhesion molecules (VCAM-1, ICAM-1, E-selectin, L-selectin) could enhance leukocyte adhesion to tumors, improving lymphocyte trafficking and boosting systemic anti-tumor effects. Lastly, HT causes vasodilation and improves blood flow, which might exacerbate those distant effects. We suggest the combination of local radiotherapy with fever-range whole-body hyperthermia to optimally enhance the chances of triggering the abscopal effect mediated by the immune system. Full article

(This article belongs to the Topic Anti-Tumor Immune Responses 2.0)

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12 pages, 636 KiB  

Open AccessArticle

Predictive Factors for Early Immune Recovery in NHL Patients after Autologous Transplantation: A Multicenter Prospective Study

by Anu Partanen, Antti Turunen, Outi Kuittinen, Hanne Kuitunen, Pentti Mäntymaa, Ville Varmavuo and Esa Jantunen

Cancers 2024, 16(14), 2550; https://doi.org/10.3390/cancers16142550 - 16 Jul 2024

Cited by 1 | Viewed by 736

Abstract

Early lymphocyte recovery as manifested by an absolute lymphocyte count at d+15 (ALC-15) ≥ 0.5 × 10⁹/L after autologous hematopoietic stem cell transplantation (AHCT) has been associated with a better outcome. This prospective multicenter study aimed to clarify factors associated with [...] Read more.

Early lymphocyte recovery as manifested by an absolute lymphocyte count at d+15 (ALC-15) ≥ 0.5 × 10⁹/L after autologous hematopoietic stem cell transplantation (AHCT) has been associated with a better outcome. This prospective multicenter study aimed to clarify factors associated with ALC-15 ≥ 0.5 × 10⁹/L after AHCT among 178 patients with non-Hodgkin lymphoma. The mobilization capacity, as manifested by peak blood CD34⁺ cell numbers > 45 × 10⁶/L correlated with higher ALC-15 levels (p = 0.020). In addition, the amount of CD3⁺CD4⁺ T cells > 31.8 × 10⁶/kg in the infused graft predicted ALC-15 ≥ 0.5 × 10⁹/L (p < 0.001). Also, the number of infused graft CD3⁺CD8⁺ T cells > 28.8 × 10⁶/kg (p = 0.017) and NK cells > 4.4 × 10⁶/kg was linked with higher ALC-15 (p < 0.001). The two-year progression-free survival after AHCT was significantly better in patients with ALC-15 ≥ 0.5 × 10⁹/L (74 vs. 57%, p = 0.027). The five-year OS in patients with higher ALC-15 was 78% vs. 60% in those with lower ALC-15 (p = 0.136). To conclude, the mobilization capacity of CD34⁺ cells and detailed measures of graft cellular content mark prognostic tools that predict ALC-15 ≥ 0.5 × 10⁹/L, which is associated with a better outcome in NHL patients after AHCT. Full article

(This article belongs to the Topic Anti-Tumor Immune Responses 2.0)

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16 pages, 3136 KiB  

Open AccessEditor’s ChoiceArticle

Anti-CD99 Antibody Therapy Triggers Macrophage-Dependent Ewing Cell Death In Vitro and Myeloid Cell Recruitment In Vivo

by Allison F. O’Neill, Evelyn M. Nguyen, Evelyn D. Maldonado, Matthew R. Chang, Jiusong Sun, Quan Zhu and Wayne A. Marasco

Antibodies 2024, 13(1), 24; https://doi.org/10.3390/antib13010024 - 18 Mar 2024

Cited by 1 | Viewed by 2545

Abstract

Background: Ewing sarcoma is a rare tumor of the bone or soft tissues characterized by diffuse membranous staining for CD99. As this tumor remains incurable in the metastatic, relapsed, and refractory settings, we explored the downstream immune implications of targeting CD99. Methods: We [...] Read more.

Background: Ewing sarcoma is a rare tumor of the bone or soft tissues characterized by diffuse membranous staining for CD99. As this tumor remains incurable in the metastatic, relapsed, and refractory settings, we explored the downstream immune implications of targeting CD99. Methods: We discovered a human anti-CD99 antibody (NOA2) by phagemid panning and investigated NOA2 immune cell-mediated cytotoxicity in vitro and in vivo focusing on the myeloid cell compartment, given that M2 macrophages are present in human tumors and associated with a poor prognosis. Results: NOA2 is capable of inducing immune effector cell-mediated Ewing death in vitro via engagement of macrophages. Mice with metastatic Ewing tumors, treated with NOA2, experience tumor growth arrest and an associated increase in intratumoral macrophages. Further, incubation of macrophages and Ewing cells with NOA2, in conjunction with anti-PILRα antibody blockade in vitro, results in the reactivation of previously dormant macrophages possibly due to interrupted binding of Ewing CD99 to macrophage PILRα. Conclusions: These studies are the first to demonstrate the role of human immune effector cells in anti-CD99-mediated Ewing tumor death. We propose that the engagement of CD99 by NOA2 results in the recruitment of intratumoral macrophages. In addition, interruption of the CD99:PILRα checkpoint axis may be a relevant therapeutic approach to activate tumor-associated macrophages. Full article

(This article belongs to the Topic Anti-Tumor Immune Responses 2.0)

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20 pages, 2300 KiB  

Open AccessReview

The Role of Tumor Metabolic Reprogramming in Tumor Immunity

by Xianhong Zhang, Weiguo Song, Yue Gao, Yu Zhang, Yuqi Zhao, Shuailin Hao and Ting Ni

Int. J. Mol. Sci. 2023, 24(24), 17422; https://doi.org/10.3390/ijms242417422 - 13 Dec 2023

Cited by 5 | Viewed by 1881

Abstract

The occurrence and development of tumors require the metabolic reprogramming of cancer cells, namely the alteration of flux in an autonomous manner via various metabolic pathways to meet increased bioenergetic and biosynthetic demands. Tumor cells consume large quantities of nutrients and produce related [...] Read more.

The occurrence and development of tumors require the metabolic reprogramming of cancer cells, namely the alteration of flux in an autonomous manner via various metabolic pathways to meet increased bioenergetic and biosynthetic demands. Tumor cells consume large quantities of nutrients and produce related metabolites via their metabolism; this leads to the remodeling of the tumor microenvironment (TME) to better support tumor growth. During TME remodeling, the immune cell metabolism and antitumor immune activity are affected. This further leads to the escape of tumor cells from immune surveillance and therefore to abnormal proliferation. This review summarizes the regulatory functions associated with the abnormal biosynthesis and activity of metabolic signaling molecules during the process of tumor metabolic reprogramming. In addition, we provide a comprehensive description of the competition between immune cells and tumor cells for nutrients in the TME, as well as the metabolites required for tumor metabolism, the metabolic signaling pathways involved, and the functionality of the immune cells. Finally, we summarize current research targeted at the development of tumor immunotherapy. We aim to provide new concepts for future investigations of the mechanisms underlying the metabolic reprogramming of tumors and explore the association of these mechanisms with tumor immunity. Full article

(This article belongs to the Topic Anti-Tumor Immune Responses 2.0)

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