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Immunological Approaches in Tumor Therapy 2.0
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Immunological Approaches in Tumor Therapy 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 6126

Special Issue Editor

Prof. Dr. Walter Fiedler

E-Mail Website
Guest Editor
Department of Oncology, Hematology and Bone Marrow Transplantation with Section Pneumology, Hubertus Wald University Cancer Center, University Medical Center Hamburg-Eppendorf, Hamburg, Germany
Interests: acute leukemia; phase 1 clinical studies; translational research
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is the continuation of our previous Special Issue “Immunological Approaches in Tumor Therapy”.

In recent years, immunotherapies have revolutionized the treatment of cancer patients. In particular, the blockade of checkpoint inhibitors such as PD-1 or CTLA4 has become a clinical routine in many cancer entities. However, the field is rapidly expanding. Many new targets and pathways have been identified that could be addressed to improve immunotherapy efficacy for better patient outcomes. In particular, new combinations of biological agents are under investigation, and interactions between tumor cells and T lymphocytes or macrophages have to be analyzed in detail in various experimental settings. Understanding the molecular and cellular basis of modifying the immune system is a prerequisite for the introduction of new therapies into the clinic.

This Special Issue, “Immunological Approaches in Tumor Therapy 2.0”, will cover a selection of recent research topics and current review articles in the field of targeting the immune system for tumor therapy.

Prof. Dr. Walter Fiedler
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • T cell
  • macrophages
  • B cell
  • PD-L1/PD-1
  • TIGIT
  • Lag-3
  • Tim-3
  • CTLA4
  • cytokines
  • receptors

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Published Papers (3 papers)

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Research

15 pages, 3853 KiB  
Article
Murine Regulatory CD4+ T Cells Are Increased in Leukemic Spleens and Show High Co-Expression of Co-Regulatory Molecules CD39, CD73, PD1, and TIGIT
by Julius Krüger, Jasmin Wellbrock, Marius Witt, Niklas Kruppa, Jana Muschhammer, Carsten Bokemeyer, Franziska Modemann, Walter Fiedler, Lena Behrmann and Franziska Brauneck
Int. J. Mol. Sci. 2024, 25(21), 11412; https://doi.org/10.3390/ijms252111412 - 24 Oct 2024
Viewed by 1254
Abstract
Comprehensive characterization of AML-associated T cells during disease progression is essential to identify relevant immune escape mechanisms and new immunotherapeutic approaches. Investigating the processes that lead to an immunosuppressive environment under progression of AML is difficult in humans, because by the time of [...] Read more.
Comprehensive characterization of AML-associated T cells during disease progression is essential to identify relevant immune escape mechanisms and new immunotherapeutic approaches. Investigating the processes that lead to an immunosuppressive environment under progression of AML is difficult in humans, because by the time of diagnosis the disease is often progressed far beyond the initial stages. Therefore, to investigate T-cell phenotypes during progression a C57BL/6 mouse model was used. The CD3+ T cells were characterized by performing multiparametric flow analyses at different time points (day 0 = healthy mice, day 7, day 14, and day 21). The study revealed that the spleen is highly infiltrated by reg CD4+ T cells at day 21 of AML progression. These spleen-infiltrating reg CD4+ T cells mainly showed an effector memory differentiation with high expression and co-expression of the checkpoint molecules TIGIT, PD-1, OX40, and the two ectoenzymes CD39 and CD73. Substantial expression of the checkpoint molecules was restricted to the central memory and effector memory compartments. Furthermore, functional evaluation of TIGIT was performed. Blocking TIGIT resulted in a significantly increased lysis of C1498 AML cells in cocultures with AML-primed CD3+ T cells. Together these data confirm that the expression of the checkpoint receptor TIGIT is relevant for dysfunction of AML-associated T cells and, thus, represents a suitable target for future immunotherapeutic approaches. Full article
(This article belongs to the Special Issue Immunological Approaches in Tumor Therapy 2.0)
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18 pages, 22139 KiB  
Article
Comparison of Follicular Helper T-Cell Markers with the Expression of the Follicular Homing Marker CXCR5 in Peripheral T-Cell Lymphomas—A Reappraisal of Follicular Helper T-Cell Lymphomas
by László Krenács, Dóra Krenács, Zita Borbényi, Erika Tóth, Anna Nagy, Klára Piukovics and Enikő Bagdi
Int. J. Mol. Sci. 2024, 25(1), 428; https://doi.org/10.3390/ijms25010428 - 28 Dec 2023
Cited by 1 | Viewed by 1451
Abstract
Peripheral T-cell lymphomas (PTCLs) expressing multiple follicular T helper (TFH) cell-related antigens are now classified as TFH lymphomas (TFHL), including angioimmunoblastic, follicular, and not otherwise specified (NOS) types. CXCR5 is the TFH cell-defining chemokine receptor that, together with its ligand CXCL13, plays a [...] Read more.
Peripheral T-cell lymphomas (PTCLs) expressing multiple follicular T helper (TFH) cell-related antigens are now classified as TFH lymphomas (TFHL), including angioimmunoblastic, follicular, and not otherwise specified (NOS) types. CXCR5 is the TFH cell-defining chemokine receptor that, together with its ligand CXCL13, plays a critical role in the development of follicles and the positioning of TFH and B cells within follicles. A comprehensive immunomorphologic study was performed to investigate the expression pattern of CXCR5 in a large cohort of nodal PTCLs, particularly those with a TFH cell phenotype, and to compare its expression with six other TFH cell-related antigens. We found that CXCR5 is widely expressed in neoplastic TFH cells, except in TFHL-NOS, and represents a specific marker of this lymphoma entity. Our results suggest that CXCR5 directs the distribution of neoplastic T cells in the affected lymph nodes and may influence the formation of the pathognomic pathological FDC network. Full article
(This article belongs to the Special Issue Immunological Approaches in Tumor Therapy 2.0)
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16 pages, 5296 KiB  
Article
The Effect of the Histone Chaperones HSPA8 and DEK on Tumor Immunity in Hepatocellular Carcinoma
by Chuanxin Yang, Yaodi Shao, Xiangjun Wang, Jie Wang, Puxiongzhi Wang, Chao Huang, Wei Wang and Jian Wang
Int. J. Mol. Sci. 2023, 24(3), 2653; https://doi.org/10.3390/ijms24032653 - 31 Jan 2023
Cited by 5 | Viewed by 2780
Abstract
Complex immune contexture leads to resistance to immunotherapy in hepatocellular carcinoma (HCC), and the need for new potential biomarkers of immunotherapy in HCC is urgent. Histone chaperones are vital determinants of gene expression and genome stability that regulate tumor development. This study aimed [...] Read more.
Complex immune contexture leads to resistance to immunotherapy in hepatocellular carcinoma (HCC), and the need for new potential biomarkers of immunotherapy in HCC is urgent. Histone chaperones are vital determinants of gene expression and genome stability that regulate tumor development. This study aimed to investigate the effect of histone chaperones on tumor immunity in HCC. Bioinformatics analyses were initially performed using The Cancer Genome Atlas (TCGA) database, and were validated using the Gene Expression Omnibus (GEO) database and the International Cancer Genome Consortium (ICGC) database. Immune-related histone chaperones were screened with the Spearman rank coefficient. Consensus clustering was utilized to divide the HCC samples into two clusters. ESTIMATE, CIBERSORT and ssGSEA analyses were performed to assess immune infiltration. The expression of immunomodulatory genes, chemokines and chemokine receptors was analyzed to evaluate sensitivity to immunotherapy. The differentially expressed genes (DEGs) were included in weighted gene coexpression network analysis (WGCNA) to identify the hub genes. Enrichment analyses were used to investigate the functions of the hub genes. The Kaplan-Meier method and log-rank test were conducted to draw survival curves. A Cox regression analysis was utilized to identify independent risk factors affecting prognosis. HSPA8 and DEK were screened out from 36 known histone chaperones based on their strongest correlation with the ESTIMATE score. Cluster 2, with high HSPA8 expression and low DEK expression, tended to have stronger immune infiltration and better sensitivity to immunotherapy than Cluster 1, with low HSPA8 expression and high DEK expression. Furthermore, WGCNA identified 12 hub genes closely correlated with immune infiltration from the DEGs of the two clusters, of which FBLN2 was proven to be an independent protective factor of HCC patients. HSPA8 and DEK are expected to be biomarkers for precisely predicting the effect of immunotherapy, and FBLN2 is expected to be a therapeutic target of HCC. Full article
(This article belongs to the Special Issue Immunological Approaches in Tumor Therapy 2.0)
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