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	4.7	9.6	2012	17.7 Days	CHF 1800	Submit
Cancers cancers	5.2	7.4	2009	17.9 Days	CHF 2900	Submit
Immuno immuno	-	-	2021	20.7 Days	CHF 1000	Submit
International Journal of Molecular Sciences ijms	5.6	7.8	2000	16.3 Days	CHF 2900	Submit
Vaccines vaccines	7.8	7.0	2013	19.2 Days	CHF 2700	Submit

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All Antibodies Cancers Immuno IJMS Vaccines

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Open AccessArticle

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

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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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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

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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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