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Journal articles on the topic 'Anti-Tumoral immunity'

Author: Grafiati

Published: 7 October 2023

Last updated: 7 July 2024

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1

Riachi, Mansour E., Carolina G. Alcantara Hirsch, Erica Ma, et al. "Abstract A018: Exercise stimulates anti-tumoral immunity in metastatic PDAC." Cancer Research 84, no. 2_Supplement (2024): A018. http://dx.doi.org/10.1158/1538-7445.panca2023-a018.

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Abstract The majority of pancreatic ductal adenocarcinoma (PDAC) patients are metastatic at presentation with limited treatment options and a poor overall 5-year survival of 3%. The liver is the predominant site of distant metastasis in PDAC. Our group has previously shown that aerobic exercise can inhibit tumorigenesis in a primary PDAC mouse model by promoting anti-tumor immunity, however, the effects of exercise in the metastatic setting have not been explored. As such, we developed a model of PDAC liver metastasis by isolating primary pancreatic and liver metastatic cell lines from 18–20-w

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Bikorimana, Jean-Pierre, Natasha Salame, Simon Beaudoin, et al. "Promoting antigen escape from dendritic cell endosomes potentiates anti-tumoral immunity." Cell Reports Medicine 3, no. 3 (2022): 100534. http://dx.doi.org/10.1016/j.xcrm.2022.100534.

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Leshem, Yasmin, Emily King, Ronit Mazor, Yoram Reiter, and Ira Pastan. "SS1P Immunotoxin Induces Markers of Immunogenic Cell Death and Enhances the Effect of the CTLA-4 Blockade in AE17M Mouse Mesothelioma Tumors." Toxins 10, no. 11 (2018): 470. http://dx.doi.org/10.3390/toxins10110470.

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SS1P is an anti-mesothelin immunotoxin composed of a targeting antibody fragment genetically fused to a truncated fragment of Pseudomonas exotoxin A. Delayed responses reported in mesothelioma patients receiving SS1P suggest that anti-tumor immunity is induced. The goal of this study is to evaluate if SS1P therapy renders mesothelioma tumors more sensitive to cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) immune checkpoint blockade. We evaluated the ability of SS1P to induce adenosine triphosphate (ATP) secretion and calreticulin expression on the surface of AE17M mouse mesothelioma cell

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Giurini, Eileena F., Mary Beth Madonna, Andrew Zloza, and Kajal H. Gupta. "Microbial-Derived Toll-like Receptor Agonism in Cancer Treatment and Progression." Cancers 14, no. 12 (2022): 2923. http://dx.doi.org/10.3390/cancers14122923.

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Toll-like receptors (TLRs) are typical transmembrane proteins, which are essential pattern recognition receptors in mediating the effects of innate immunity. TLRs recognize structurally conserved molecules derived from microbes and damage-associated molecular pattern molecules that play an important role in inflammation. Since the first discovery of the Toll receptor by the team of J. Hoffmann in 1996, in Drosophila melanogaster, numerous TLRs have been identified across a wide range of invertebrate and vertebrate species. TLR stimulation leads to NF-κB activation and the subsequent production

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Rivera-Molina, Yisel, Juan Fueyo, Hong Jiang, et al. "EXTH-27. ACTIVATING THE IMMUNITY WITHIN THE TUMOR USING VIROIMMUNOTHERAPY: DELTA-24-RGD ONCOLYTIC ADENOVIRUS ARMED WITH THE IMMUNOPOSITIVE REGULATOR GITRL." Neuro-Oncology 21, Supplement_6 (2019): vi87. http://dx.doi.org/10.1093/neuonc/noz175.359.

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Abstract Based on promising results of recent clinical trials using oncolytic viruses, virotherapy is evolving as an alternative to treat patients with malignant glioma. Our group developed the oncolytic adenovirus Delta-24-RGD (DNX-2401) that is being tested, alone or in combination with anti-PD1, in clinical trials for recurrent glioblastoma (NCT00805376; NCT01956734; NCT02798406). The results suggest that, besides the expected oncolytic effect, the injection of the pathogen initiated, in a subset of patients, an anti-tumoral immunity that led to 20% of long-term survivors (3.5–5 years). To

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Cohen-Solal, Joel F. G., Lydie Cassard, Emilie M. Fournier, Shannon M. Loncar, Wolf Herman Fridman, and Catherine Sautès-Fridman. "Metastatic Melanomas Express Inhibitory Low Affinity Fc Gamma Receptor and Escape Humoral Immunity." Dermatology Research and Practice 2010 (2010): 1–11. http://dx.doi.org/10.1155/2010/657406.

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Our research, inspired by the pioneering works of Isaac Witz in the 1980s, established that 40% of human metastatic melanomas express ectopically inhibitory Fc gamma receptors (FcRIIB), while they are detected on less than 5% of primary cutaneous melanoma and not on melanocytes. We demonstrated that these tumoral FcRIIB act as decoy receptors that bind the Fc portion of antimelanoma IgG, which may prevent Fc recognition by the effector cells of the immune system and allow the metastatic melanoma to escape the humoral/natural immune response. The FcRIIB is able to inhibit the ADCC (antibody dep

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Mirlekar, Bhalchandra, and Yuliya Pylayeva-Gupta. "Abstract PO-019: Reprogramming of naïve B cells in pancreatic cancer subverts humoral immunity." Cancer Research 81, no. 22_Supplement (2021): PO—019—PO—019. http://dx.doi.org/10.1158/1538-7445.panca21-po-019.

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Abstract B cells frequently infiltrate human tumors, and the intra-tumoral abundance of plasma cells can correlate with improved patient prognosis. However, many tumors are devoid of plasma B cells, and strategies to enhance anti-tumor B cell responses are needed. We report the existence of a negative regulatory signaling network that reprograms naïve B cells in pancreatic cancer to antagonize anti-tumor plasma B cells. This network is driven by IL-35-mediated STAT3 activation, which directly stimulates upregulation of the pioneer transcription factors Pax5 and Bcl6 in naïve B cells and impede

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Geidel, G., M. Maurer, T. Luger, and K. Loser. "649 OX40/OX40L and 4-1BB/4-1BBL signaling in cutaneous anti-tumoral immunity." Journal of Investigative Dermatology 136, no. 5 (2016): S115. http://dx.doi.org/10.1016/j.jid.2016.02.690.

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Wu, Deyang, Xiaowei Liu, Jingtian Mu, Jin Yang, Fanglong Wu, and Hongmei Zhou. "Therapeutic Approaches Targeting Proteins in Tumor-Associated Macrophages and Their Applications in Cancers." Biomolecules 12, no. 3 (2022): 392. http://dx.doi.org/10.3390/biom12030392.

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Tumor-associated macrophages (TAMs) promote tumor proliferation, invasion, angiogenesis, stemness, therapeutic resistance, and immune tolerance in a protein-dependent manner. Therefore, the traditional target paradigms are often insufficient to exterminate tumor cells. These pro-tumoral functions are mediated by the subsets of macrophages that exhibit canonical protein markers, while simultaneously having unique transcriptional features, which makes the proteins expressed on TAMs promising targets during anti-tumor therapy. Herein, TAM-associated protein-dependent target strategies were develo

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Remsik, Jan, Xinran Tong, Min Jun Li, et al. "LMD-16. Choroid plexus orchestrates anti-cancer immunity in leptomeninges." Neuro-Oncology Advances 3, Supplement_3 (2021): iii10—iii11. http://dx.doi.org/10.1093/noajnl/vdab071.041.

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Abstract Choroid plexus (CP) forms an anatomically functional barrier between the blood and cerebrospinal fluid (CSF) that dictates the cellular and humoral composition of the CSF. The immunological response of CP to inflammatory stimuli, such as cancer, remains unclear. Here, we find that CP orchestrates the immune composition of CSF in the steady state as well as in the presence of metastatic cancer. We show that the circulation-derived leptomeningeal monocyte-macrophages entering the CSF through CP promote the growth of leptomeningeal metastasis (LM) by perturbing the environment with a sto

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Revel, Margot, Marie V. Daugan, Catherine Sautés-Fridman, Wolf H. Fridman, and Lubka T. Roumenina. "Complement System: Promoter or Suppressor of Cancer Progression?" Antibodies 9, no. 4 (2020): 57. http://dx.doi.org/10.3390/antib9040057.

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Constituent of innate immunity, complement is present in the tumor microenvironment. The functions of complement include clearance of pathogens and maintenance of homeostasis, and as such could contribute to an anti-tumoral role in the context of certain cancers. However, multiple lines of evidence show that in many cancers, complement has pro-tumoral actions. The large number of complement molecules (over 30), the diversity of their functions (related or not to the complement cascade), and the variety of cancer types make the complement-cancer topic a very complex matter that has just started

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Lee, Eun Jung, Da Hyeon Yun, Seungpil Jung, and Serk In Park. "Abstract 2191: Alteration of anti-tumoral immunity in the pre-metastatic bone microenvironment via autonomic nerve system dysfunction." Cancer Research 82, no. 12_Supplement (2022): 2191. http://dx.doi.org/10.1158/1538-7445.am2022-2191.

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Abstract Bone metastasis is a major cause of morbidity and mortality for breast cancer patients. Bone is a unique metastatic microenvironment because of complex interactions among numerous distinct cell types such as osteo-blasts, -clasts, -cytes and marrow immune cells in physiological and pathological conditions. Imbalanced bone homeostasis by diverse factors such as the sympathetic nerve system (SNS) activation, potentially contribute to the progression of bone metastasis, yet precise mechanisms remain unclear. We investigated the effects of beta 2 adrenergic receptor (β2AR) activation in o

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Wang, Xuefeng, Xin Gao, Xin Zhao, et al. "Tumoral expression of IL-33 promotes Anti-tumor Immune Responses (TUM2P.912)." Journal of Immunology 192, no. 1_Supplement (2014): 71.36. http://dx.doi.org/10.4049/jimmunol.192.supp.71.36.

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Abstract One major approach of cancer immune therapy is to convert the tumor immunosuppressive microenvironment to one that favors antitumor immune responses. We have recently demonstrated that Interleukin 33 (IL-33) promotes effector functions of CD8 T cells, suggesting a potential function in antitumor immunity. Here we showed that overexpression of IL-33 in two tumor cell lines, 4T1 and B16, potently inhibited tumor growth in vivo. CD45+, CD8+ T cells, NK cells, IFN-γ+ CD8+ T cells and IFN-γ+ NK cells were greatly increased in the IL-33-expressing tumors when compared with those in the cont

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Brummer, Christina, Tobias Pukrop, Joachim Wiskemann, Christina Bruss, Ines Ugele, and Kathrin Renner. "Can Exercise Enhance the Efficacy of Checkpoint Inhibition by Modulating Anti-Tumor Immunity?" Cancers 15, no. 18 (2023): 4668. http://dx.doi.org/10.3390/cancers15184668.

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Immune checkpoint inhibition (ICI) has revolutionized cancer therapy. However, response to ICI is often limited to selected subsets of patients or not durable. Tumors that are non-responsive to checkpoint inhibition are characterized by low anti-tumoral immune cell infiltration and a highly immunosuppressive tumor microenvironment. Exercise is known to promote immune cell circulation and improve immunosurveillance. Results of recent studies indicate that physical activity can induce mobilization and redistribution of immune cells towards the tumor microenvironment (TME) and therefore enhance a

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Zerdes, Wallerius, Sifakis, et al. "STAT3 Activity Promotes Programmed-Death Ligand 1 Expression and Suppresses Immune Responses in Breast Cancer." Cancers 11, no. 10 (2019): 1479. http://dx.doi.org/10.3390/cancers11101479.

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Signal transducer and activator of transcription 3 (STAT3) is an oncogene and multifaceted transcription factor involved in multiple cellular functions. Its role in modifying anti-tumor immunity has been recently recognized. In this study, the biologic effects of STAT3 on immune checkpoint expression and anti-tumor responses were investigated in breast cancer (BC). A transcriptional signature of phosphorylated STAT3 was positively correlated with PD-L1 expression in two independent cohorts of early BC. Pharmacologic inhibition and gene silencing of STAT3 led to decreased Programmed Death Ligan

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Rosato, Pamela, Jianfang Ning, Noah Veis Gavil, et al. "Functional virus-specific memory CD8+ T cells survey glioblastoma." Journal of Immunology 208, no. 1_Supplement (2022): 121.15. http://dx.doi.org/10.4049/jimmunol.208.supp.121.15.

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Abstract Glioblastoma multiforme (GBM) is among the most aggressive, treatment resistant cancers, and despite standard of care surgery, radiation and chemotherapy, is invariably fatal. GBM is marked by local and systemic immunosuppression, contributing to resistance to existing immunotherapies that have had success in other tumor types. Memory T cells specific for previous infections reside in tissues throughout the host, including the brain, and are capable of rapid and potent immune activation. Here, we show that virus-specific memory CD8+ T cells expressing tissue resident markers populate

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Kendal, Joseph K., Michael S. Shehata, Serena Y. Lofftus, and Joseph G. Crompton. "Cancer-Associated B Cells in Sarcoma." Cancers 15, no. 3 (2023): 622. http://dx.doi.org/10.3390/cancers15030622.

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Despite being one of the first types of cancers studied that hinted at a major role of the immune system in pro- and anti-tumor biology, little is known about the immune microenvironment in sarcoma. Few types of sarcoma have shown major responses to immunotherapy, and its rarity and heterogeneity makes it challenging to study. With limited systemic treatment options, further understanding of the underlying mechanisms in sarcoma immunity may prove crucial in advancing sarcoma care. While great strides have been made in the field of immunotherapy over the last few decades, most of these efforts

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Veneziani, Irene, Claudia Alicata, Lorenzo Moretta, and Enrico Maggi. "The Latest Approach of Immunotherapy with Endosomal TLR Agonists Improving NK Cell Function: An Overview." Biomedicines 11, no. 1 (2022): 64. http://dx.doi.org/10.3390/biomedicines11010064.

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Toll-like receptors (TLRs) are the most well-defined pattern recognition receptors (PRR) of several cell types recognizing pathogens and triggering innate immunity. TLRs are also expressed on tumor cells and tumor microenvironment (TME) cells, including natural killer (NK) cells. Cell surface TLRs primarily recognize extracellular ligands from bacteria and fungi, while endosomal TLRs recognize microbial DNA or RNA. TLR engagement activates intracellular pathways leading to the activation of transcription factors regulating gene expression of several inflammatory molecules. Endosomal TLR agonis

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Araújo, Thaise Gonçalves, Sara Teixeira Soares Mota, Helen Soares Valença Ferreira, Matheus Alves Ribeiro, Luiz Ricardo Goulart, and Lara Vecchi. "Annexin A1 as a Regulator of Immune Response in Cancer." Cells 10, no. 9 (2021): 2245. http://dx.doi.org/10.3390/cells10092245.

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Annexin A1 is a 37 kDa phospholipid-binding protein that is expressed in many tissues and cell types, including leukocytes, lymphocytes and epithelial cells. Although Annexin A1 has been extensively studied for its anti-inflammatory activity, it has been shown that, in the cancer context, its activity switches from anti-inflammatory to pro-inflammatory. Remarkably, Annexin A1 shows pro-invasive and pro-tumoral properties in several cancers either by eliciting autocrine signaling in cancer cells or by inducing a favorable tumor microenvironment. Indeed, the signaling of the N-terminal peptide o

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Kim, Do-Hyun, Sangho Lim, Hong-Gyun Lee, Chun Geun Lee, Jack A. Elias, and Je-Min Choi. "Regulation of Chitinase-3-like-1 in T cell enhances anti-tumoral T cell responses to suppress lung metastasis." Journal of Immunology 200, no. 1_Supplement (2018): 57.27. http://dx.doi.org/10.4049/jimmunol.200.supp.57.27.

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Abstract Chitinase-3-like-1 (Chi3l1) is known to play a significant role in the pathogenesis of Type 2 inflammation and cancer. However, the function of Chi3l1 in T cell and its clinical implications are largely unknown. Here we showed that Chi3l1 expression was increased in Th2 cells while it decreased in Th1 cells by time dependent manner. In addition, Chi3l1-deficient T cells were hyper-responsive to TcR stimulation and were prone to differentiating into Th1 cells, and retroviral transduction of Chi3l1 rescue increased IFNγ expression in Chi3l1-deficient Th1 cells. Chi3l1-deficient Th1 cell

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Trandafir, Maria-Florina, Octavian Savu, Daniela Pasarica, Coralia Bleotu, and Mihaela Gheorghiu. "Interleukin-6 as a Director of Immunological Events and Tissue Regenerative Capacity in Hemodialyzed Diabetes Patients." Medical Sciences 12, no. 2 (2024): 31. http://dx.doi.org/10.3390/medsci12020031.

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Hemodialyzed patients have innate immunity activation and adaptive immunity senescence. Diabetes mellitus is a frequent cause for chronic kidney disease and systemic inflammation. We studied the immunological pattern (innate and acquired immunity) and the tissular regeneration capacity in two groups of hemodialyzed patients: one comprised of diabetics and the other of non-diabetics. For inflammation, the following serum markers were determined: interleukin 6 (IL-6), interleukin 1β (IL-1β), tumoral necrosis factor α (TNF-α), IL-6 soluble receptor (sIL-6R), NGAL (human neutrophil gelatinase-asso

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Qiao, Rong, Rong Xiao, Zhong Chen, et al. "Cloning, Expression and Inhibitory Effects on Lewis Lung Carcinoma Cells of rAj-Tspin from Sea Cucumber (Apostichopus japonicus)." Molecules 27, no. 1 (2021): 229. http://dx.doi.org/10.3390/molecules27010229.

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In recent years, sea cucumber has become a favorite healthcare food due to its characteristic prevention of cardiovascular diseases, suppression of tumors, as well as enhancement of immunity. In order to screen the anti-tumoral proteins or peptides from sea cucumber (Apostichopus japonicus), its cDNA library was analyzed, and a disintegrin-like and metalloproteinase with thrombospondin type 1 motif, member 13 (ADAMTS13)-like was found. ADAMTS13-like contains 10 thrombospondin 1 (TSP1) domains. Based on analysis of bioinformatics, the third TSP1 domain of this protein, which is further named Aj

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Mori, Shiori, Rina Fujiwara-Tani, Shingo Kishi та ін. "Enhancement of Anti-Tumoral Immunity by β-Casomorphin-7 Inhibits Cancer Development and Metastasis of Colorectal Cancer". International Journal of Molecular Sciences 22, № 15 (2021): 8232. http://dx.doi.org/10.3390/ijms22158232.

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β-Casomorphin-7 (BCM) is a degradation product of β-casein, a milk component, and has been suggested to affect the immune system. However, its effect on mucosal immunity, especially anti-tumor immunity, in cancer-bearing individuals is not clear. We investigated the effects of BCM on lymphocytes using an in vitro system comprising mouse splenocytes, a mouse colorectal carcinogenesis model, and a mouse orthotopic colorectal cancer model. Treatment of mouse splenocytes with BCM in vitro reduced numbers of cluster of differentiation (CD) 20+ B cells, CD4+ T cells, and regulatory T cells (Tregs),

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Kim, Hyun-Jin, Jang Hyun Park, Hyeon Cheol Kim, Chae Won Kim, In Kang, and Heung Kyu Lee. "Blood monocyte-derived CD169+ macrophages contribute to antitumor immunity against glioblastoma." Journal of Immunology 210, no. 1_Supplement (2023): 84.11. http://dx.doi.org/10.4049/jimmunol.210.supp.84.11.

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Abstract Infiltrating tumor-associated macrophages (TAM) are known to impede immunotherapy against glioblastoma (GBM), however, TAMs are heterogeneous, and there are no clear markers to distinguish immunosuppressive and potentially immune-activating populations. Here we identify a subset of CD169+ macrophages promoting an anti-tumoral microenvironment in GBM. Using single-cell transcriptome analysis, we find that CD169+ macrophages in human and mouse gliomas produce pro-inflammatory chemokines, leading to the accumulation of T cells and NK cells. CD169 expression on macrophages facilitates pha

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Beissert, S., S. Grabbe, M. Voskort, T. A. Luger, T. Schwarz, and R. D. Granstein. "Effects of senescence on induction and elicitation of protective anti-tumoral immunity by langerhans cells in mice." Journal of Dermatological Science 16 (March 1998): S90. http://dx.doi.org/10.1016/s0923-1811(98)83534-2.

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Charrier, Emily, Rémi Vernet, Frank Schwenter, Patricia Luy, Alena Donda, and Nicolas Mach. "A Functional GM-CSF Receptor on Dendritic Cells Is Required for Efficient Protective Anti-Tumor Immunity." Immuno 1, no. 3 (2021): 240–52. http://dx.doi.org/10.3390/immuno1030016.

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Dendritic cells (DC) play a major role during the priming phase of anti-tumor immunization, as they are required for an efficient tumor-associated antigens presentation. At least one dendritic cell-based therapy has already been successfully approved by regulators for clinical application in prostate cancer patients. Moreover, DC development is dependent on the granulocyte macrophage colony stimulating factor (GM-CSF), a cytokine that has been successfully used as a potent inducer of anti-tumoral immunity. To better understand the relation between DC and GM-CSF in anti-tumor immunity, we studi

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Kim, Seon-Hee, Chungyong Han, Byoung S. Kwon та Beom K. Choi. "CD4 depletion potentiates anti-tumor immunity in adoptive immunotherapy by increasing IL-18Rαhi endogenous CD8+ T cells". Journal of Immunology 204, № 1_Supplement (2020): 170.7. http://dx.doi.org/10.4049/jimmunol.204.supp.170.7.

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Abstract Adoptive T cell therapy (ACT) requires lympho-depletion pre-conditioning to eliminate immune-suppressive elements to allow for the efficient engraftment of adoptively transferred tumor-reactive T cells. Because anti-CD4 monoclonal antibody depletes CD4+ immune-suppressive cells to enhance anti-tumor immunity, combinations of anti-CD4 treatment and ACT have synergistic potential in cancer therapy. We designed a post-ACT conditioning regimen that involves weekly treatment with anti-CD4 (CD4post). Using murine melanoma, cyclophosphamide and tumor-reactive CD8+ T cell infusion were includ

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Bishani, Ali, and Elena L. Chernolovskaya. "Activation of Innate Immunity by Therapeutic Nucleic Acids." International Journal of Molecular Sciences 22, no. 24 (2021): 13360. http://dx.doi.org/10.3390/ijms222413360.

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Nucleic acid-based therapeutics have gained increased attention during recent decades because of their wide range of application prospects. Immunostimulatory nucleic acids represent a promising class of potential drugs for the treatment of tumoral and viral diseases due to their low toxicity and stimulation of the body’s own innate immunity by acting on the natural mechanisms of its activation. The repertoire of nucleic acids that directly interact with the components of the immune system is expanding with the improvement of both analytical methods and methods for the synthesis of nucleic acid

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Zhang, Tao, Yu Wang, Qing Li та ін. "Mesenchymal stromal cells equipped by IFNα empower T cells with potent anti-tumor immunity". Oncogene 41, № 13 (2022): 1866–81. http://dx.doi.org/10.1038/s41388-022-02201-4.

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AbstractCancer treatments have been revolutionized by the emergence of immune checkpoint blockade therapies. However, only a minority of patients with various tumor types have benefited from such treatments. New strategies focusing on the immune contexture of the tumor tissue microenvironment hold great promises. Here, we created IFNα-overexpressing mesenchymal stromal cells (IFNα-MSCs). Upon direct injection into tumors, we found that these cells are powerful in eliminating several types of tumors. Interestingly, the intra-tumoral injection of IFNα-MSCs could also induce specific anti-tumor e

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Rafei, M., J. Abusarah, and R. Shammaa. "The next generation cancer vaccines: genetically engineered mesenchymal stromal cells exhibit robust anti-tumoral immunity surpassing dendritic cells." Cytotherapy 22, no. 5 (2020): S31. http://dx.doi.org/10.1016/j.jcyt.2020.03.015.

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Cho, Jeong Hyun, Hyo-Ji Lee, Hyun-Jeong Ko, et al. "The TLR7 agonist imiquimod induces anti-cancer effects via autophagic cell death and enhances anti-tumoral and systemic immunity during radiotherapy for melanoma." Oncotarget 8, no. 15 (2017): 24932–48. http://dx.doi.org/10.18632/oncotarget.15326.

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Pandey, Sanjay, Claudia G. Chavez, Indranil Basu, Andy Minn, and Chandan Guha. "Abstract 3444: Administration of anti-CD40 enhances local and systemic antitumor efficacy of radiotherapy in allograft tumor model of a check-point blockade resistant melanoma." Cancer Research 82, no. 12_Supplement (2022): 3444. http://dx.doi.org/10.1158/1538-7445.am2022-3444.

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Abstract Resistance to immune checkpoint therapy develops in a subset of patients after initial response. Therefore, we hypothesized that defective antigen presentation contributes to immune resistance, and a sequential therapy comprising of ablative radiation therapy (RT) and agonist αCD40 antibody can reprogram the tumor-infiltrating myeloid and dendritic cells for effective in-situ tumor antigen presentation and activation of T cells. Palpable B16-F10-Res499 tumors in C57BL/6 mice, resistant to the systemic effects of RT and αCTLA-4 blockade, were treated with 3 fractions of 20Gy (RT) follo

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Poccia, F., B. Cipriani, S. Vendetti, et al. "CD94/NKG2 inhibitory receptor complex modulates both anti-viral and anti-tumoral responses of polyclonal phosphoantigen-reactive V gamma 9V delta 2 T lymphocytes." Journal of Immunology 159, no. 12 (1997): 6009–17. http://dx.doi.org/10.4049/jimmunol.159.12.6009.

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Abstract Viral, bacterial, protozoal, and cancer-associated Ags elicit strong responses in human gammadelta T lymphocytes. The majority of these cells in the peripheral blood express the Vgamma9Vdelta2-encoded TCR and recognize nonpeptidic phosphoantigens without an apparent MHC restriction. We have shown that Vgamma9Vdelta2 T cells express the inhibitory CD94/NKG2 receptor for HLA class I molecules. The anti-CD94 mAb inhibits 1) the Vgamma9Vdelta2 T cell proliferation in response mycobacterial phosphoantigens and 2) the HIV-induced Vgamma9Vdelta2 T cell expansion. Vgamma9Vdelta2 T cells stimu

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Liu, Haiyan. "Differential roles of tumoral and systemic IL-1α in the development of hepatocellular carcinoma". Journal of Immunology 200, № 1_Supplement (2018): 178.24. http://dx.doi.org/10.4049/jimmunol.200.supp.178.24.

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Abstract Interleukin-1α (IL-1α) is a pro-inflammatory cytokine that has been shown to be up-regulated in many tumors. However, the role of IL-1α during tumor development is still not clear. IL-1α could be released by necrotic tumor cells passively to the tumor microenvironment or by other cells actively during inflammation. In the current study, we investigated the role of secreted IL-1α released in the tumor microenvironment or systemically in the tumor development using murine hepatocellular carcinoma (HCC) models. We constructed murine HCC hepa1-6 cells stably expressing secreted IL-1α and

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Dorrier, Cayce, Felagot Abebe, Olivia Pak, Emily De-Bodene, and Joshua Wang. "Abstract LB117: Virus-inspired Particles (ViPs) harnessing cytomegalovirus immune memory for local and systemic cancer immunotherapy." Cancer Research 84, no. 7_Supplement (2024): LB117. http://dx.doi.org/10.1158/1538-7445.am2024-lb117.

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Abstract VerImmune is pioneering a First-in-Class treatment known as “Anti-tumor Immune Redirection” (AIR). This approach repurposes a patient’s pre-existing anti-viral or childhood vaccine immunity towards tumor cells for targeted destruction. VerImmune’s lead product, VERI-101, leverages pre-existing CD8+ T-cell immune memory acquired from past human cytomegalovirus (HCMV) infections. VERI-101 consists of VerImmune’s proprietary platform technology known as ViPs (Virus-inspired Particles) that are conjugated on their surface with a CD8+ T cell viral peptide antigen. ViPs are based on a modif

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Awasthi, Deepika, and Aditya Sarode. "Neutrophils at the Crossroads: Unraveling the Multifaceted Role in the Tumor Microenvironment." International Journal of Molecular Sciences 25, no. 5 (2024): 2929. http://dx.doi.org/10.3390/ijms25052929.

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Over the past decade, research has prominently established neutrophils as key contributors to the intricate landscape of tumor immune biology. As polymorphonuclear granulocytes within the innate immune system, neutrophils play a pivotal and abundant role, constituting approximately ∼70% of all peripheral leukocytes in humans and ∼10–20% in mice. This substantial presence positions them as the frontline defense against potential threats. Equipped with a diverse array of mechanisms, including reactive oxygen species (ROS) generation, degranulation, phagocytosis, and the formation of neutrophil e

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Cannon, Anthony Michael, and Mark H. Kaplan. "IL-9 responsive macrophages utilize Arginase 1 to enhance lung tumor growth." Journal of Immunology 210, no. 1_Supplement (2023): 84.09. http://dx.doi.org/10.4049/jimmunol.210.supp.84.09.

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Abstract In cancer, the immunosuppressive function of myeloid cells that support tumor progression is controlled by secreted factors in the tumor microenvironment. In the tumor microenvironment, arginine and arginine-derived metabolites have been demonstrated to be crucial factors in tumor development. Within macrophages, arginine metabolism influences the polarization of macrophages and therefore, tumor growth by eliciting an anti-tumoral or pro-tumoral phenotype. Interleukin 9 (IL-9) is a pleiotropic cytokine that signals through the IL-9 receptor (IL-9R) and can function as a positive or ne

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Lan, Keng-Hsueh, Ying-Chun Sheng, Keng-Li Lan, KyungMann Kim, Sung-Hsin Kuo, and Zachary Morris. "Abstract 1098: Combination of a DNA vaccine-induced immune checkpoint blockade and radiation therapy induces anti-tumor immunity." Cancer Research 83, no. 7_Supplement (2023): 1098. http://dx.doi.org/10.1158/1538-7445.am2023-1098.

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Abstract Background: Immune checkpoint blockade (ICB) immunotherapy improves survival for many cancer patients, but those with immunologically ‘cold’ tumors do not derive benefit. Radiation therapy (RT) has been demonstrated to augment antitumor immunity in preclinical and clinical studies and may enhance response to ICB in immunologically cold tumors. We have developed DNA-based, cost-effective, and versatile ICB immunotherapies. Here, we test the use of these alone and in combination with RT as a novel treatment approach in syngeneic murine melanoma models. Materials and methods: We construc

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Hoelzinger, Dominique, Ana Dominguez, Kevin Pollock, Joseph Lustgarten, Peter Cohen, and Sandra Gendler. "IL-9 strategy to perturb Treg function and enhance anti-tumor immunity (P4273)." Journal of Immunology 190, no. 1_Supplement (2013): 140.9. http://dx.doi.org/10.4049/jimmunol.190.supp.140.9.

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Abstract IL-9 is a cytokine that is primarily associated with mast cells and airway inflammation, however it also plays a role in T regulatory cell (Treg) survival and recruitment to tumors. We previously reported that 4-1BB treatment of Tregs inhibits both Treg function and IL-9 secretion. Neutralization of IL-9 with an anti-IL-9 antibody inhibits the suppressive function of Tregs without affecting the function of CD4+ and CD8+ T effector cells. Furthermore, the combination of intra-tumoral CpG and anti-IL-9 induced tumor rejection in BALB-neuT and MUC1 tolerant transgenic mice. Here we show

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Niavarani, Seyedeh Raheleh, Christine Lawson, and Lee-Hwa Tai. "Treatment of Metastatic Disease through Natural Killer Cell Modulation by Infected Cell Vaccines." Viruses 11, no. 5 (2019): 434. http://dx.doi.org/10.3390/v11050434.

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Oncolytic viruses (OVs) are a form of immunotherapy that release tumor antigens in the context of highly immunogenic viral signals following tumor-targeted infection and destruction. Emerging preclinical and clinical evidence suggests that this in situ vaccine effect is critical for successful viro-immunotherapy. In this review, we discuss the application of OV as an infected cell vaccine (ICV) as one method of enhancing the potency and breadth of anti-tumoral immunity. We focus on understanding and manipulating the critical role of natural killer (NK) cells and their interactions with other i

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Carrel, Sabrina, Michelle Li, Batul Al-Zubeidy, et al. "Abstract A028: Disparities in suppressive immunity in Hispanic/Latina patients with hormone receptor positive breast cancer." Cancer Research 84, no. 3_Supplement_1 (2024): A028. http://dx.doi.org/10.1158/1538-7445.advbc23-a028.

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Abstract In the US, breast cancer is the number one cancer diagnosed, and it is responsible for the most cancer related deaths among Hispanic/Latina (H/L) women. The mean age of diagnosis of breast cancer in H/L patients is 3.7 years younger than their Non-Hispanic White (NHW) counterparts. Despite being diagnosed with breast cancer at a younger age, the H/L population has a better overall survival rate across all breast cancer subtypes. This study investigates whether the immune response mounted against tumor cells in the H/L population differs from that mounted by NHW patients. We recruited

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Everts, Anne, Melissa Bergeman, Grant McFadden, and Vera Kemp. "Simultaneous Tumor and Stroma Targeting by Oncolytic Viruses." Biomedicines 8, no. 11 (2020): 474. http://dx.doi.org/10.3390/biomedicines8110474.

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Current cancer therapeutics often insufficiently eradicate malignant cells due to the surrounding dense tumor stroma. This multi-componential tissue consists of mainly cancer-associated fibroblasts, the (compact) extracellular matrix, tumor vasculature, and tumor-associated macrophages, which all exert crucial roles in maintaining a pro-tumoral niche. Their continuous complex interactions with tumor cells promote tumor progression and metastasis, emphasizing the challenges in tumor therapy development. Over the last decade, advances in oncolytic virotherapy have shown that oncolytic viruses (O

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Tiemeijer, Bart M., Lucie Descamps, Jesse Hulleman, Jelle J. F. Sleeboom, and Jurjen Tel. "A Microfluidic Approach for Probing Heterogeneity in Cytotoxic T-Cells by Cell Pairing in Hydrogel Droplets." Micromachines 13, no. 11 (2022): 1910. http://dx.doi.org/10.3390/mi13111910.

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Cytotoxic T-cells (CTLs) exhibit strong effector functions to leverage antigen-specific anti-tumoral and anti-viral immunity. When naïve CTLs are activated by antigen-presenting cells (APCs) they display various levels of functional heterogeneity. To investigate this, we developed a single-cell droplet microfluidics platform that allows for deciphering single CTL activation profiles by multi-parameter analysis. We identified and correlated functional heterogeneity based on secretion profiles of IFNγ, TNFα, IL-2, and CD69 and CD25 surface marker expression levels. Furthermore, we strengthened o

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Peggs, Karl S., Sergio A. Quezada, Tyler R. Simpson, and James P. Allison. "Dissociation of Systemic and Local Anti-Tumor Immunity Following Depletion of Regulatory T Cells Limits Therapeutic Activity in Established Tumors." Blood 110, no. 11 (2007): 286. http://dx.doi.org/10.1182/blood.v110.11.286.286.

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Abstract Interference with the inhibitory immunological checkpoints controlling T-cell activation provides new opportunities to augment cancer immunotherapies. CD4+CD25+Foxp3+ T cells (Treg) are important regulators of T cell activity being largely responsible for the maintenance of peripheral self-tolerance. Evidence for their role in fostering immune privilege within tumors has fueled attempts to manipulate their number or function for therapeutic benefit. In pre-clinical tumor models, CD25-directed Treg depletion efficiently synergizes with various immune-based approaches but only when depl

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Saito, Yasuyuki, Satomi Komori, Takenori Kotani, Yoji Murata, and Takashi Matozaki. "The Role of Type-2 Conventional Dendritic Cells in the Regulation of Tumor Immunity." Cancers 14, no. 8 (2022): 1976. http://dx.doi.org/10.3390/cancers14081976.

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Conventional dendritic cells (cDCs) orchestrate immune responses to cancer and comprise two major subsets: type-1 cDCs (cDC1s) and type-2 cDCs (cDC2s). Compared with cDC1s, which are dedicated to the activation of CD8+ T cells, cDC2s are ontogenically and functionally heterogeneous, with their main function being the presentation of exogenous antigens to CD4+ T cells for the initiation of T helper cell differentiation. cDC1s play an important role in tumor-specific immune responses through cross-presentation of tumor-derived antigens for the priming of CD8+ T cells, whereas little is known of

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Orlandella, Rachael M., Shannon Boi, Daniel Smith, and Lyse A. Norian. "Understanding the effects of a calorie restriction mimetic on renal cancer progression and CD8 T cell immunity." Journal of Immunology 198, no. 1_Supplement (2017): 76.12. http://dx.doi.org/10.4049/jimmunol.198.supp.76.12.

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Abstract Metastatic renal cell carcinoma (RCC) exhibits high mortality rates and chemotherapeutic resistance. Immune-based therapies, including high-dose IL-2 and anti-PD1, are efficacious in ~20% of patients; however, both are associated with substantial toxicity. This highlights the need for additional research aimed at improving response rates while also limiting toxicity. Previous findings by other groups have demonstrated that nutrient deprivation prior to chemotherapy reduces treatment toxicity and may improve therapeutic efficacy in cancer patients. Recent murine research shows that die

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Crescenzi, Elvira, Antonio Leonardi, and Francesco Pacifico. "NGAL as a Potential Target in Tumor Microenvironment." International Journal of Molecular Sciences 22, no. 22 (2021): 12333. http://dx.doi.org/10.3390/ijms222212333.

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The signaling network between cancer and stromal cells plays a crucial role in tumor microenvironment. The fate of tumor progression mainly depends on the huge amount of information that these cell populations exchange from the onset of neoplastic transformation. Interfering with such signaling has been producing exciting results in cancer therapy: just think of anti-PD-1/anti-PD-L1/anti-CTLA-4 antibodies that, acting as immune checkpoint inhibitors, interrupt the inhibitory signaling exerted by cancer cells on immune cells or the CAR-T technology that fosters the reactivation of anti-tumoral

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Guth, Amanda, Emily Monk, Rajesh Agarwal, et al. "Targeting Fat Oxidation in Mouse Prostate Cancer Decreases Tumor Growth and Stimulates Anti-Cancer Immunity." International Journal of Molecular Sciences 21, no. 24 (2020): 9660. http://dx.doi.org/10.3390/ijms21249660.

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Lipid catabolism represents an Achilles heel in prostate cancer (PCa) that can be exploited for therapy. CPT1A regulates the entry of fatty acids into the mitochondria for beta-oxidation and its inhibition has been shown to decrease PCa growth. In this study, we examined the pharmacological blockade of lipid oxidation with ranolazine in TRAMPC1 PCa models. Oral administration of ranolazine (100 mg/Kg for 21 days) resulted in decreased tumor CD8+ T-cells Tim3 content, increased macrophages, and decreased blood myeloid immunosuppressive monocytes. Using multispectral staining, drug treatments in

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Cano, Carla E., Christine Pasero, Aude De Gassart, et al. "BTN2A, a New Immune-Checkpoint Targeting Vg9Vd2 T Cell Cytotoxicity." Blood 134, Supplement_1 (2019): 1044. http://dx.doi.org/10.1182/blood-2019-128658.

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Background: Anti-tumoral response of Vg9Vd2 T cells requires sensing of phosphoantigens accumulated in malignant cells through binding of butyrophilin 3A(BTN3A). Moreover, an unknown partner located in human Chr6 was shown to be mandatory to BTN3A-mediated Vg9Vd2 T cell activation in murine models. Here, we identified butyrophilin 2A (BTN2A), which is located to Chr6, as a requirement for BTN3A-mediated Vg9Vd2 T cell cytotoxicity against cancer cells. Methods: CRISPR-Cas9-mediated inactivation of BTN2A1/2A2 isoforms was performed in Daudi, K562 and HEK-293T cells. Vg9Vd2 T cells expanded from

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Bruno, Gennaro, Nicoletta Nastasi, Angela Subbiani та ін. "Abstract 3887: β3-adrenergic receptor sustains IFN-γ-dependent PD-L1 expression and impairs anti-tumor immunity in neuroblastoma". Cancer Research 82, № 12_Supplement (2022): 3887. http://dx.doi.org/10.1158/1538-7445.am2022-3887.

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Abstract In this study we aimed to investigate the role of the β3-adrenergic receptor (β3-AR) in regulating the immune system response against neuroblastoma (NB) tumor. NB is a very heterogeneous extracranial tumor occurring in childhood. A distinctive feature of NB tumors is their neuroendocrine ability to secrete catecholamines, which in turn, via β-adrenergic receptors ligation, may affect different signaling pathways in the tumor microenvironment (TME). We previously demonstrated that the specific antagonism of the β3-AR on NB tumor cells affected tumor growth and progression. Here, in a m

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