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Targeting Innate Immunity to Treat Cancer

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A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Immunology and Immunotherapy".

Deadline for manuscript submissions: closed (31 July 2021) | Viewed by 71472

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Prof. Dr. Harriet Kluger

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Guest Editor

Medical Oncology, Yale School of Medicine, 333 Cedar St, WWW211B, New Haven, CT 06520, USA
Interests: melanoma; renal cell carcinoma; brain metastasis; immunotherapy

Special Issue Information

Dear Colleagues,

Inhibitors of PD-1, its ligand, and CTLA-4 have dramatically changed cancer care for many tumor types. These are generally thought to enhance cytotoxic T cell activity. Innate immunity, however, also plays a key role in tumor rejection, and extensive studies, both clinical and preclinical, are currently underway to boost innate immunity in the treatment of cancer.

The innate immune system involves a number of cell types in addition to physical barriers. Macrophages, monocytes, neutrophils, basophils, dendritic cells, and subsets of T cells such as NK cells play key roles in innate immunity. These cellular subsets may be activated by immune checkpoint inhibitors but also express co-stimulatory molecules that can be harnessed for cancer therapy. Moreover, they are activated by specific cytokines that can similarly be used to treat cancer.

In this Special Issue, we review key cell types involved in innate immunity. Select, promising molecules that enhance innate immunity are discussed. Finally, cutting-edge technologies that can further our understanding of complex immune interactions at the cellular level are reviewed.

Prof. Harriet Kluger
Guest Editor

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Keywords

macrophages
monocytes
dendritic cells
natural killer cells
metabolism
tumor microenvironment
CD40
CD47/SIRPα
single cell technologies

Published Papers (13 papers)

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Editorial

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2 pages, 160 KiB

Open AccessEditorial

Targeting Innate Immunity to Treat Cancer

by Matthew Austin and Harriet Kluger

Cancers 2020, 12(10), 2723; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers12102723 - 23 Sep 2020

Cited by 1 | Viewed by 1512

Abstract

In recent years, it has become clear that the immune system plays a critical role in rejecting malignant cells [...] Full article

(This article belongs to the Special Issue Targeting Innate Immunity to Treat Cancer)

Research

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23 pages, 3751 KiB

Open AccessArticle

3D Model of the Early Melanoma Microenvironment Captures Macrophage Transition into a Tumor-Promoting Phenotype

by Gabriela A. Pizzurro, Chang Liu, Kathryn Bridges, Amanda F. Alexander, Alice Huang, Janani P. Baskaran, Julie Ramseier, Marcus W. Bosenberg, Michael Mak and Kathryn Miller-Jensen

Cancers 2021, 13(18), 4579; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13184579 - 12 Sep 2021

Cited by 6 | Viewed by 4544

Abstract

Tumor immune response is shaped by the tumor microenvironment (TME), which often evolves to be immunosuppressive, promoting disease progression and metastasis. An important example is melanoma tumors, which display high numbers of tumor-associated macrophages (TAMs) that are immunosuppressive but also have the potential to restore anti-tumor activity. However, to therapeutically target TAMs, there is a need to understand the early events that shape their tumor-promoting profile. To address this, we built and optimized 3D in vitro co-culture systems, composed of a collagen-I matrix scaffolding murine bone-marrow-derived macrophages (BMDMs), YUMM1.7 melanoma cells, and fibroblasts to recreate the early melanoma TME and study how interactions with fibroblasts and tumor cells modulate macrophage immune activity. We monitored BMDM behavior and interactions through time-lapse imaging and characterized their activation and secretion. We found that stromal cells induced a rapid functional activation, with increased motility and response from BMDMs. Over the course of seven days, BMDMs acquired a phenotype and secretion profile that resembled melanoma TAMs in established tumors. Overall, the direct cell–cell interactions with the stromal components in a 3D environment shape BMDM transition to a TAM-like immunosuppressive state. Our systems will enable future studies of changes in macrophage–stromal cross-talk in the melanoma TME. Full article

(This article belongs to the Special Issue Targeting Innate Immunity to Treat Cancer)

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15 pages, 2622 KiB

Open AccessArticle

Identification of Immune Cell Infiltration in Murine Pheochromocytoma during Combined Mannan-BAM, TLR Ligand, and Anti-CD40 Antibody-Based Immunotherapy

by Ondrej Uher, Thanh-Truc Huynh, Boqun Zhu, Lucas A. Horn, Veronika Caisova, Katerina Hadrava Vanova, Rogelio Medina, Herui Wang, Claudia Palena, Jindrich Chmelar, Zhengping Zhuang, Jan Zenka and Karel Pacak

Cancers 2021, 13(16), 3942; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13163942 - 05 Aug 2021

Cited by 5 | Viewed by 2317

Abstract

Immunotherapy has become an essential component in cancer treatment. However, the majority of solid metastatic cancers, such as pheochromocytoma, are resistant to this approach. Therefore, understanding immune cell composition in primary and distant metastatic tumors is important for therapeutic intervention and diagnostics. Combined mannan-BAM, TLR ligand, and anti-CD40 antibody-based intratumoral immunotherapy (MBTA therapy) previously resulted in the complete eradication of murine subcutaneous pheochromocytoma and demonstrated a systemic antitumor immune response in a metastatic model. Here, we further evaluated this systemic effect using a bilateral pheochromocytoma model, performing MBTA therapy through injection into the primary tumor and using distant (non-injected) tumors to monitor size changes and detailed immune cell infiltration. MBTA therapy suppressed the growth of not only injected but also distal tumors and prolonged MBTA-treated mice survival. Our flow cytometry analysis showed that MBTA therapy led to increased recruitment of innate and adaptive immune cells in both tumors and the spleen. Moreover, adoptive CD4⁺ T cell transfer from successfully MBTA-treated mice (i.e., subcutaneous pheochromocytoma) demonstrates the importance of these cells in long-term immunological memory. In summary, this study unravels further details on the systemic effect of MBTA therapy and its use for tumor and metastasis reduction or even elimination. Full article

(This article belongs to the Special Issue Targeting Innate Immunity to Treat Cancer)

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23 pages, 2961 KiB

Open AccessArticle

Distinct Responsiveness of Tumor-Associated Macrophages to Immunotherapy of Tumors with Different Mechanisms of Major Histocompatibility Complex Class I Downregulation

by Adrianna Piatakova, Ingrid Polakova, Jana Smahelova, Shweta Dilip Johari, Jaroslav Nunvar and Michal Smahel

Cancers 2021, 13(12), 3057; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13123057 - 19 Jun 2021

Cited by 4 | Viewed by 2516

Abstract

Tumor-associated macrophages (TAMs) plentifully infiltrate the tumor microenvironment (TME), but their role in anti-tumor immunity is controversial. Depending on the acquired polarization, they can either support tumor growth or participate in the elimination of neoplastic cells. In this study, we analyzed the TME by RNA-seq and flow cytometry and examined TAMs after ex vivo activation. Tumors with normal and either reversibly or irreversibly decreased expression of major histocompatibility complex class I (MHC-I) molecules were induced with TC-1, TC-1/A9, and TC-1/dB2m cells, respectively. We found that combined immunotherapy (IT), composed of DNA immunization and the CpG oligodeoxynucleotide (ODN) ODN1826, evoked immune reactions in the TME of TC-1- and TC-1/A9-induced tumors, while the TME of TC-1/dB2m tumors was mostly immunologically unresponsive. TAMs infiltrated both tumor types with MHC-I downregulation, but only TAMs from TC-1/A9 tumors acquired the M1 phenotype upon IT and were cytotoxic in in vitro assay. The anti-tumor effect of combined IT was markedly enhanced by a blockade of the colony-stimulating factor-1 receptor (CSF-1R), but only against TC-1/A9 tumors. Overall, TAMs from tumors with irreversible MHC-I downregulation were resistant to the stimulation of cytotoxic activity. These data suggest the dissimilarity of TAMs from different tumor types, which should be considered when utilizing TAMs in cancer IT. Full article

(This article belongs to the Special Issue Targeting Innate Immunity to Treat Cancer)

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15 pages, 2581 KiB

Open AccessArticle

Plasmacytoid Dendritic Cell (pDC) Infiltration Correlate with Tumor Infiltrating Lymphocytes, Cancer Immunity, and Better Survival in Triple Negative Breast Cancer (TNBC) More Strongly than Conventional Dendritic Cell (cDC)

by Masanori Oshi, Stephanie Newman, Yoshihisa Tokumaru, Li Yan, Ryusei Matsuyama, Pawel Kalinski, Itaru Endo and Kazuaki Takabe

Cancers 2020, 12(11), 3342; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers12113342 - 12 Nov 2020

Cited by 62 | Viewed by 3940

Abstract

Dendritic cells (DC) represent a major antigen-presenting cell type in the tumor immune microenvironment (TIME) and play an essential role in cancer immunity. Conventional DC (cDC) and plasmacytoid DC (pDC) were defined by the xCell algorithm and a total of 2968 breast cancer patients (TCGA and METABRIC) were analyzed. We found that triple-negative breast cancer (TNBC) had a high fraction of cDC and pDC compared to the other subtypes. In contrast to cDC, high pDC in TNBC was significantly associated with better disease-specific and disease-free survival consistently in both cohorts. High cDC TNBC tumors enriched not only inflammation and immune-related, but also metastasis-related gene sets in Gene Set Enrichment Analysis, whereas high pDC TNBC enriched inflammation and immune -related gene sets including IFN-γ signaling more strongly than cDC. pDC TNBC correlated with CD8⁺, CD4⁺ memory, IFN-γ score, and cytolytic activity stronger than cDC TNBC. High pDC TNBC were associated with a high fraction of anti-cancer immune cells and high expression of all the immune check point molecules examined. In conclusion, pDC levels correlated with the infiltration of immune cells and patient survival in TNBC more strongly than cDC; this is the first study suggesting the clinical relevance of pDC infiltration in TNBC. Full article

(This article belongs to the Special Issue Targeting Innate Immunity to Treat Cancer)

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Review

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17 pages, 702 KiB

Open AccessReview

Cancer Therapy Targeting CD47/SIRPα

by Nazli Dizman and Elizabeth I. Buchbinder

Cancers 2021, 13(24), 6229; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13246229 - 11 Dec 2021

Cited by 20 | Viewed by 4862

Abstract

In the past decade, the field of cancer immunotherapy has rapidly advanced, establishing a crucial role for immune checkpoint blockers in the treatment of a variety of cancer types. In parallel with these remarkable clinical developments, further efforts have focused on ways of unleashing adaptive immune responses against cancer. CD47, a cell surface molecule overexpressed by several cancer types that facilitates immune escape from macrophages, dendritic cells and natural killer cells, and its ligand SIRPα, have emerged as potential therapeutic targets. A number of agents directed to CD47/SIRPα have been developed and demonstrated preclinical activity. Early phase clinical trials are investigating CD47/SIRPα directed agents with available data, suggesting safety and preliminary activity. Herein, we provide an overview of the mechanistic rationale of targeting CD47/SIRPα axis and associated clinical evidence. Full article

(This article belongs to the Special Issue Targeting Innate Immunity to Treat Cancer)

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14 pages, 1030 KiB

Open AccessFeature PaperReview

Overcoming Immunotherapy Resistance by Targeting the Tumor-Intrinsic NLRP3-HSP70 Signaling Axis

by Balamayooran Theivanthiran, Tarek Haykal, Linda Cao, Alisha Holtzhausen, Michael Plebanek, Nicholas C. DeVito and Brent A. Hanks

Cancers 2021, 13(19), 4753; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13194753 - 23 Sep 2021

Cited by 9 | Viewed by 2839

Abstract

The tumor-intrinsic NOD-like receptor family, pyrin-domain-containing-3 (NLRP3) inflammasome, plays an important role in regulating immunosuppressive myeloid cell populations in the tumor microenvironment (TME). While prior studies have described the activation of this inflammasome in driving pro-tumorigenic mechanisms, emerging data is now revealing the tumor NLRP3 inflammasome and the downstream release of heat shock protein-70 (HSP70) to regulate anti-tumor immunity and contribute to the development of adaptive resistance to anti-PD-1 immunotherapy. Genetic alterations that influence the activity of the NLRP3 signaling axis are likely to impact T cell-mediated tumor cell killing and may indicate which tumors rely on this pathway for immune escape. These studies suggest that the NLRP3 inflammasome and its secreted product, HSP70, represent promising pharmacologic targets for manipulating innate immune cell populations in the TME while enhancing responses to anti-PD-1 immunotherapy. Additional studies are needed to better understand tumor-specific regulatory mechanisms of NLRP3 to enable the development of tumor-selective pharmacologic strategies capable of augmenting responses to checkpoint inhibitor immunotherapy while minimizing unwanted off-target effects. The execution of upcoming clinical trials investigating this strategy to overcome anti-PD-1 resistance promises to provide novel insight into the role of this pathway in immuno-oncology. Full article

(This article belongs to the Special Issue Targeting Innate Immunity to Treat Cancer)

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23 pages, 964 KiB

Open AccessReview

The Role of Tumor-Associated Macrophages in Hematologic Malignancies

by Emanuele Cencini, Alberto Fabbri, Anna Sicuranza, Alessandro Gozzetti and Monica Bocchia

Cancers 2021, 13(14), 3597; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13143597 - 18 Jul 2021

Cited by 34 | Viewed by 3672

Abstract

The tumor microenvironment includes dendritic cells, T-cytotoxic, T-helper, reactive B-lymphoid cells and macrophages; these reactive cells could interplay with malignant cells and promote tumor growth and survival. Among its cellular components, tumor-associated macrophages (TAM) represent a component of the innate immune system and play an important role, especially in hematologic malignancies. Depending on the stimuli that trigger their activation, TAM are polarized towards form M1, contributing to antitumor responses, or M2, associated with tumor progression. Many studies demonstrated a correlation between TAM, disease progression and the patient’s outcome in lymphoproliferative neoplasms, such as Hodgkin lymphoma (HL) and non-Hodgkin lymphoma (NHL), even if with conflicting results. A critical hurdle to overcome is surely represented by the heterogeneity in the choice of the optimal markers and methods used for TAM analysis (gene-expression profile vs. immunohistochemistry, CD163vs. CD68vs. CD163/CD68 double-positive cells). TAM have been recently linked to the development and progression of multiple myeloma and leukemia, with a critical role in the homing of malignant cells, drug resistance, immune suppression and angiogenesis. As such, this review will summarize the role of TAM in different hematologic malignancies, focusing on the complex interplay between TAM and tumor cells, the prognostic value of TAM and the possible TAM-targeted therapeutic strategies. Full article

(This article belongs to the Special Issue Targeting Innate Immunity to Treat Cancer)

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24 pages, 790 KiB

Open AccessEditor’s ChoiceReview

STING Agonists as Cancer Therapeutics

by Afsaneh Amouzegar, Manoj Chelvanambi, Jessica N. Filderman, Walter J. Storkus and Jason J. Luke

Cancers 2021, 13(11), 2695; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13112695 - 30 May 2021

Cited by 176 | Viewed by 19376

Abstract

The interrogation of intrinsic and adaptive resistance to cancer immunotherapy has identified lack of antigen presentation and type I interferon signaling as biomarkers of non-T-cell-inflamed tumors and clinical progression. A myriad of pre-clinical studies have implicated the cGAS/stimulator of interferon genes (STING) pathway, a cytosolic DNA-sensing pathway that drives activation of type I interferons and other inflammatory cytokines, in the host immune response against tumors. The STING pathway is also increasingly understood to have other anti-tumor functions such as modulation of the vasculature and augmentation of adaptive immunity via the support of tertiary lymphoid structure development. Many natural and synthetic STING agonists have entered clinical development with the first generation of intra-tumor delivered cyclic dinucleotides demonstrating safety but only modest systemic activity. The development of more potent and selective STING agonists as well as novel delivery systems that would allow for sustained inflammation in the tumor microenvironment could potentially augment response rates to current immunotherapy approaches and overcome acquired resistance. In this review, we will focus on the latest developments in STING-targeted therapies and provide an update on the clinical development and application of STING agonists administered alone, or in combination with immune checkpoint blockade or other approaches. Full article

(This article belongs to the Special Issue Targeting Innate Immunity to Treat Cancer)

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16 pages, 2058 KiB

Open AccessReview

Pediatric Tumors-Mediated Inhibitory Effect on NK Cells: The Case of Neuroblastoma and Wilms’ Tumors

by Andrea Pelosi, Piera Filomena Fiore, Sabina Di Matteo, Irene Veneziani, Ignazio Caruana, Stefan Ebert, Enrico Munari, Lorenzo Moretta, Enrico Maggi and Bruno Azzarone

Cancers 2021, 13(10), 2374; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13102374 - 14 May 2021

Cited by 12 | Viewed by 2620

Abstract

Natural killer (NK) cells play a key role in the control of cancer development, progression and metastatic dissemination. However, tumor cells develop an array of strategies capable of impairing the activation and function of the immune system, including NK cells. In this context, a major event is represented by the establishment of an immunosuppressive tumor microenvironment (TME) composed of stromal cells, myeloid-derived suppressor cells, tumor-associated macrophages, regulatory T cells and cancer cells themselves. The different immunoregulatory cells infiltrating the TME, through the release of several immunosuppressive molecules or by cell-to-cell interactions, cause an impairment of the recruitment of NK cells and other lymphocytes with effector functions. The different mechanisms by which stromal and tumor cells impair NK cell function have been particularly explored in adult solid tumors and, in less depth, investigated and discussed in a pediatric setting. In this review, we will compare pediatric and adult solid malignancies concerning the respective mechanisms of NK cell inhibition, highlighting novel key data in neuroblastoma and Wilms’ tumor, two of the most frequent pediatric extracranial solid tumors. Indeed, both tumors are characterized by the presence of stromal cells acting through the release of immunosuppressive molecules. In addition, specific tumor cell subsets inhibit NK cell cytotoxic function by cell-to-cell contact mechanisms likely controlled by the transcriptional coactivator TAZ. These findings could lead to a more performant diagnostic approach and to the development of novel immunotherapeutic strategies targeting the identified cellular and molecular targets. Full article

(This article belongs to the Special Issue Targeting Innate Immunity to Treat Cancer)

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13 pages, 648 KiB

Open AccessReview

Harnessing Natural Killer Cells in Cancer Immunotherapy: A Review of Mechanisms and Novel Therapies

by Frederique St-Pierre, Shailender Bhatia and Sunandana Chandra

Cancers 2021, 13(8), 1988; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13081988 - 20 Apr 2021

Cited by 15 | Viewed by 6222

Abstract

Natural killer (NK) cells are lymphocytes that are integral to the body’s innate immunity, resulting in a rapid immune response to stressed or infected cells in an antigen-independent manner. The innate immune system plays an important role in the recognition of tumor-derived stress-related factors and is critical to subsequent adaptive immune responses against tumor antigens. The aim of this review is to discuss mechanisms by which tumor cells evade NK cells and to outline strategies that harness NK cells for cancer immunotherapy. We discuss strategies to relieve the exhausted state of NK cells, recent therapies focused on targeting NK-cell-specific activating and inhibitory receptors, the use of cytokines IL-2 and IL-15 to stimulate autologous or allogeneic NK cells, and ongoing trials exploring the use of genetically modified NK cells and chimeric antigen-receptor-modified NK (CAR-NK) cells. Full article

(This article belongs to the Special Issue Targeting Innate Immunity to Treat Cancer)

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18 pages, 647 KiB

Open AccessEditor’s ChoiceReview

Agonistic CD40 Antibodies in Cancer Treatment

by Dijana Djureinovic, Meina Wang and Harriet M. Kluger

Cancers 2021, 13(6), 1302; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13061302 - 15 Mar 2021

Cited by 48 | Viewed by 9952

Abstract

CD40 is expressed on a variety of antigen-presenting cells. Stimulation of CD40 results in inflammation by upregulation of other costimulatory molecules, increased antigen presentation, maturation (licensing) of dendritic cells, and activation of CD8+ T cells. Here we analyzed gene expression data from The Cancer Genome Atlas in melanoma, renal cell carcinoma, and pancreatic adenocarcinoma and found correlations between CD40 and several genes involved in antigen presentation and T cell function, supporting further exploration of CD40 agonists to treat cancer. Agonist CD40 antibodies have induced anti-tumor effects in several tumor models and the effect has been more pronounced when used in combination with other treatments (immune checkpoint inhibition, chemotherapy, and colony-stimulating factor 1 receptor inhibition). The reduction in tumor growth and ability to reprogram the tumor microenvironment in preclinical models lays the foundation for clinical development of agonistic CD40 antibodies (APX005M, ChiLob7/4, ADC-1013, SEA-CD40, selicrelumab, and CDX-1140) that are currently being evaluated in early phase clinical trials. In this article, we focus on CD40 expression and immunity in cancer, agonistic human CD40 antibodies, and their pre-clinical and clinical development. With the broad pro-inflammatory effects of CD40 and its ligand on dendritic cells and macrophages, and downstream B and T cell activation, agonists of this pathway may enhance the anti-tumor activity of other systemic therapies. Full article

(This article belongs to the Special Issue Targeting Innate Immunity to Treat Cancer)

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23 pages, 1862 KiB

Open AccessEditor’s ChoiceReview

Metabolism of Innate Immune Cells in Cancer

by Ronan Talty and Kelly Olino

Cancers 2021, 13(4), 904; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13040904 - 21 Feb 2021

Cited by 26 | Viewed by 5394

Abstract

Cancer cells possess specific metabolic requirements for their survival, proliferation, and progression. Within a shared microenvironment, immune cells depend on competing metabolic pathways for their development and effector function. As a result, local acidification, hypoxia, and nutrient depletion in the tumor microenvironment can alter the antitumor immune response and even promote resistance to immunotherapies such as immune checkpoint blockade and adoptive cell transfer. Although T cells are the primary effectors of the antitumor response, growing evidence demonstrates that innate immune cells are critical to successful tumor clearance. This review aims to summarize current research related to the innate immune system, metabolism, and cancer. We first discuss the specific metabolic requirements of innate immune cells for immune activation and suppression and conclude by highlighting ongoing clinical applications of these findings. Full article

(This article belongs to the Special Issue Targeting Innate Immunity to Treat Cancer)

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