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Relevant bibliographies by topics / NK cell therapy

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Academic literature on the topic 'NK cell therapy'

Author: Grafiati

Published: 9 March 2023

Last updated: 10 March 2023

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Journal articles on the topic "NK cell therapy"

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Verma, Divya, Mukesh Verma, and Rangnath Mishra. "Stem Cell Therapy and Innate Lymphoid Cells." Stem Cells International 2022 (August 2, 2022): 1–12. http://dx.doi.org/10.1155/2022/3530520.

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Innate lymphoid cells have the capability to communicate with other immune cell types to coordinate the immune system functioning during homeostasis and inflammation. However, these cells behave differently at the functional level, unlike T cells, these cells do not need antigen receptors for activation because they are activated by the interaction of their receptor ligation. In hematopoietic stem cell transplantation (HSCT), T cells and NK cells have been extensively studied but very few studies are available on ILCs. In this review, an attempt has been made to provide current information related to NK and ILCs cell-based stem cell therapies and role of the stem cells in the regulation of ILCs as well. Also, the latest information on the differentiation of NK cells and ILCs from CD34+ hematopoietic stem cells is covered in the article.

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Wang, Hua, Bi-bo Fu, Robert Peter Gale, and Yang Liang. "NK-/T-cell lymphomas." Leukemia 35, no. 9 (June 11, 2021): 2460–68. http://dx.doi.org/10.1038/s41375-021-01313-2.

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AbstractNatural killer/T-cell lymphoma (NKTL) is a sub-type of Epstein–Barr virus (EBV)-related non-Hodgkin lymphomas common in Asia and Latin America but rare elsewhere. Its pathogenesis is complex and incompletely understood. Lymphoma cells are transformed from NK- or T-cells, sometimes both. EBV-infection and subsequent genetic alterations in infected cells are central to NKTL development. Hemophagocytic syndrome is a common complication. Accurate staging is important to predict outcomes but there is controversy which system is best. More than two-thirds of NKTL lympohmas are localized at diagnosis, are frequently treated with radiation therapy only and have 5-year survival of about 70 percent. Persons with advanced NKTLs receive radiation therapy synchronously or metachronously with diverse multi-drug chemotherapy typically including l-asparginase with 5-year survival of about 40 percent. Some persons with widespread NKTL receive chemotherapy only. There are few data on safety and efficacy of high-dose therapy and a haematopoietic cell autotransplant. Immune therapies, histone deacetylase (HDAC)-inhibitors and other drugs are in early clinical trials. There are few randomized controlled clinical trials in NKTLs and no therapy strategy is clearly best; more effective therapy(ies) are needed. Some consensus recommendations are not convincingly evidence-based. Mechanisms of multi-drug resistance are considered. We discuss these issues including recent advances in our understanding of and therapy of NKTLs.

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Lachota, Mieszko, Marianna Vincenti, Magdalena Winiarska, Kjetil Boye, Radosław Zagożdżon, and Karl-Johan Malmberg. "Prospects for NK Cell Therapy of Sarcoma." Cancers 12, no. 12 (December 11, 2020): 3719. http://dx.doi.org/10.3390/cancers12123719.

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Natural killer (NK) cells are innate lymphoid cells with potent antitumor activity. One of the most NK cell cytotoxicity-sensitive tumor types is sarcoma, an aggressive mesenchyme-derived neoplasm. While a combination of radical surgery and radio- and chemotherapy can successfully control local disease, patients with advanced sarcomas remain refractory to current treatment regimens, calling for novel therapeutic strategies. There is accumulating evidence for NK cell-mediated immunosurveillance of sarcoma cells during all stages of the disease, highlighting the potential of using NK cells as a therapeutic tool. However, sarcomas display multiple immunoevasion mechanisms that can suppress NK cell function leading to an uncontrolled tumor outgrowth. Here, we review the current evidence for NK cells’ role in immune surveillance of sarcoma during disease initiation, promotion, progression, and metastasis, as well as the molecular mechanisms behind sarcoma-mediated NK cell suppression. Further, we apply this basic understanding of NK–sarcoma crosstalk in order to identify and summarize the most promising candidates for NK cell-based sarcoma immunotherapy.

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Xiao, Jiani, Tianxiang Zhang, Fei Gao, Zhengwei Zhou, Guang Shu, Yizhou Zou, and Gang Yin. "Natural Killer Cells: A Promising Kit in the Adoptive Cell Therapy Toolbox." Cancers 14, no. 22 (November 17, 2022): 5657. http://dx.doi.org/10.3390/cancers14225657.

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As an important component of the innate immune system, natural killer (NK) cells have gained increasing attention in adoptive cell therapy for their safety and efficacious tumor-killing effect. Unlike T cells which rely on the interaction between TCRs and specific peptide-MHC complexes, NK cells are more prone to be served as “off-the-shelf” cell therapy products due to their rapid recognition and killing of tumor cells without MHC restriction. In recent years, constantly emerging sources of therapeutic NK cells have provided flexible options for cancer immunotherapy. Advanced genetic engineering techniques, especially chimeric antigen receptor (CAR) modification, have yielded exciting effectiveness in enhancing NK cell specificity and cytotoxicity, improving in vivo persistence, and overcoming immunosuppressive factors derived from tumors. In this review, we highlight current advances in NK-based adoptive cell therapy, including alternative sources of NK cells for adoptive infusion, various CAR modifications that confer different targeting specificity to NK cells, multiple genetic engineering strategies to enhance NK cell function, as well as the latest clinical research on adoptive NK cell therapy.

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Hurton, Lenka, R. Iram Siddik, Harjeet Singh, Simon Olivares, Brian Rabinovich, William Hildebrand, Dean Lee, et al. "Identifying NK-Cell Donors for Cell Therapy Based on Functional Phenotype." Blood 110, no. 11 (November 16, 2007): 3271. http://dx.doi.org/10.1182/blood.v110.11.3271.3271.

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Abstract Donor natural killer (NK) cells after haploidentical hematopoietic stem-cell transplantation (HSCT) and infusion of haploidentical NK-cells have demonstrated a therapeutic effect. NK alloreactivity resulting from appropriate Killer cell Ig-like receptor (KIR)-ligand disparity in human-leukocyte-antigen (HLA)-haplotype mismatched HSCT has resulted in improved engraftment and decreased incidence of leukemia relapse. Yet, not all patient-donor pairs benefit for an allogeneic NK-cell effect. To identify NK-cell donors with a suitable KIR-ligand mismatch, we have developed a functional assay to measure NK-cell killing through KIR-ligand interactions. NK-cell lysis of target cells is blocked by inhibitory KIR that recognize classical HLA class I allotypes and HLA mismatches of an altered allelic repertoire, as in haploidentical HSCT, leading to KIR-ligand mismatch and alloreactive NK cell-mediated target killing (Figure 1A). A cytotoxicity assay was developed based on the NK-cell target HLAnull 721.221 cells, and a panel of targets with enforced expression of HLA genes recognized by KIR. After the killing assay was optimized for high throughput and sensitivity, we used the panel of targets to determine whether bulk populations of donor NK cells could be predicted to kill based on KIR and HLA typing. The results demonstrate patterns of target-cell lysis for the KIR repertoires corresponding, for some donors, with predicted donor-versus-recipient NK-cell alloreactivity (Figure 1B). A relative inhibition of HLA+ target-cell lysis of >30% was associated with binding of KIR to introduced HLA class I molecules. The benefit of this assay to transplant physicians is a tool to actually measure phenotype (lysis), rather than relying on predictive models based on genotype. This assay will be combined with typing data to help identify donors with NK-cell killing function for recipients of haploidentical HSCT and infusion of haploidentical NK cells. Figure 1. (A) Schematic of alloreactivity generated between NK cells that are KIR-ligand mismatched with targets. (B) Observed lysis of 721.221 cells, with enforced expression of HLA class I, by KIR-typed donar(box). Figure 1. (A) Schematic of alloreactivity generated between NK cells that are KIR-ligand mismatched with targets. (B) Observed lysis of 721.221 cells, with enforced expression of HLA class I, by KIR-typed donar(box).

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Parameswaran, Reshmi, David N. Wald, Marcos De Lima, Dean A. Lee, and Stephen Moreton. "Novel Approach for NK Cell Therapy for Cancer." Blood 124, no. 21 (December 6, 2014): 3836. http://dx.doi.org/10.1182/blood.v124.21.3836.3836.

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Abstract Novel therapeutic approaches are urgently needed for many malignancies such as Acute Myeloid Leukemia (AML). We have developed a new therapeutic strategy based upon NK cell immunotherapy that exhibits high clinical potential based upon cell and animal studies. While the harnessing of NK cells for cellular therapy against malignancies has been a topic of interest for several decades, our approach overcomes a major hurdle of insufficient NK cell cytotoxic activity. We have identified that targeting the kinase GSK3 through pharmacologic and genetic approaches leads to the hyperactivation of human blood derived NK cells and a significant improvement in efficacy as compared to traditionally used activated NK cells or chemotherapy in our mouse AML model systems. Importantly this GSK3 inhibition can be achieved through a short ex-vivo incubation of NK cells with a GSK3 inhibitor paving the way for a rapid implementation into a clinical trial. Utilizing both in vitro studies with AML cell lines (ex. OCI-AML3 and HL-60)) and primary human AML cells we observe approximately a 50% increase in efficacy with GSK3 inhibited NK cells as compared to untreated NK cells. Further, we demonstrate significant efficacy of GSK3 inhibited NK cells in a mouse model of circulating human AML. After 4 weekly injections of human NK cells, there is a 50% greater reduction in human AML cells present in the mouse bone marrow with GSK3 inhibited NK cells as compared to vehicle treated NK cells. Besides efficacy studies, our work has led a model of how GSK3-inhibition enhances NK cell activity as depicted in figure 1. GSK3 inhibition leads to a dramatic increase in adhesion of NK cells to target cells as demonstrated by a flow cytometric adhesion assay (49% vs 83% after 20 min incubation) as well as live cell imaging. Consistent with the increased adhesion, GSK3 inhibited NK cells as well as target cells (after co-incubation) exhibit increased expression of essential NK cell-target adhesion molecules including L-selectin (on NK cells) and ICAM (on target cells). The induction of ICAM on target cells is due to a marked induction in TNFa production from the NK cells upon incubation with target cells (>7 fold increase in TNFa production). TNFa neutralization impairs the NK activity of the GSK3 inhibited NK cells (~30%) but not vehicle treated cells. Finally, GSK3 inhibition also leads to changes in the NK cells that enhance activity such as increased expression of granzyme and perforin and secretion of IFNg. Overall, our work has a revealed a novel strategy for NK cell therapy that holds high clinical potential. Figure 1. Model of how GSK3 inhibition leads to hyperactive NK cells. GSK3I - GSK3 inhibitor Figure 1. Model of how GSK3 inhibition leads to hyperactive NK cells. GSK3I - GSK3 inhibitor Disclosures No relevant conflicts of interest to declare.

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Liberatore, Concetta, Marusca Capanni, Nicola Albi, Isabella Volpi, Elena Urbani, Loredana Ruggeri, Amedea Mencarelli, Francesco Grignani, and Andrea Velardi. "Natural Killer Cell–mediated Lysis of Autologous Cells Modified by Gene Therapy." Journal of Experimental Medicine 189, no. 12 (June 21, 1999): 1855–62. http://dx.doi.org/10.1084/jem.189.12.1855.

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This study investigated the role of natural killer (NK) cells as effectors of an immune response against autologous cells modified by gene therapy. T lymphocytes were transduced with LXSN, a retroviral vector adopted for human gene therapy that carries the selectable marker gene neo, and the autologous NK response was evaluated. We found that (i) infection with LXSN makes cells susceptible to autologous NK cell–mediated lysis; (ii) expression of the neo gene is responsible for conferring susceptibility to lysis; (iii) lysis of neo-expressing cells is clonally distributed and mediated only by NK clones that exhibit human histocompatibility leukocyte antigen (HLA)-Bw4 specificity and bear KIR3DL1, a Bw4-specific NK inhibitory receptor; and (iv) the targets are cells from HLA-Bw4+ individuals. Finally, neo peptides anchoring to the Bw4 allele HLA-B27 interfered with KIR3DL1-mediated recognition of HLA-B27, i.e., they triggered NK lysis. Moreover, neo gene mutations preventing translation of two of the four potentially nonprotective peptides reduced KIR3DL1+ NK clone–mediated autologous lysis. Thus, individuals expressing Bw4 alleles possess an NK repertoire with the potential to eliminate autologous cells modified by gene therapy. By demonstrating that NK cells can selectively detect the expression of heterologous genes, these observations provide a general model of the NK cell–mediated control of viral infections.

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Valamehr, Bahram. "Advancing iPSC-derived NK cell therapy." Cell and Gene Therapy Insights 5, no. 12 (December 18, 2019): 1655–61. http://dx.doi.org/10.18609/cgti.2019.173.

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Mehta, Rohtesh S., Brion Randolph, May Daher, and Katayoun Rezvani. "NK cell therapy for hematologic malignancies." International Journal of Hematology 107, no. 3 (January 27, 2018): 262–70. http://dx.doi.org/10.1007/s12185-018-2407-5.

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Chu, Yaya, Margaret Lamb, Mitchell S. Cairo, and Dean A. Lee. "The Future of Natural Killer Cell Immunotherapy for B Cell Non-Hodgkin Lymphoma (B Cell NHL)." Current Treatment Options in Oncology 23, no. 3 (March 2022): 381–403. http://dx.doi.org/10.1007/s11864-021-00932-2.

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Opinion statementNatural killer (NK) cells have played a critical—if largely unrecognized or ignored—role in the treatment of B cell non-Hodgkin lymphoma (NHL) since the introduction of CD20-directed immunotherapy with rituximab as a cornerstone of therapy over 25 years ago. Engagement with NK cells leading to lysis of NHL targets through antibody-dependent cellular cytotoxicity (ADCC) is a critical component of rituximab’s mechanism of action. Despite this important role, the only aspect of B cell NHL therapy that has been adopted as standard therapy that even indirectly augments or restores NK cell function is the introduction of obinutuzumab, a CD20 antibody with enhanced ability to engage with NK cells. However, over the last 5 years, adoptive immunotherapy with effector lymphocytes of B cell NHL has experienced tremendous growth, with five different CAR T cell products now licensed by the FDA, four of which target CD19 and have approved indications for some subtype of B cell NHL—axicabtagene ciloleucel, brexucabtagene autoleucel, lisocabtagene maraleucel, and tisagenlecleucel. These T cell-based immunotherapies essentially mimic the recognition, activation pathway, and cytotoxic machinery of a CD19 antibody engaging NK cells and lymphoma targets. Despite their efficacy, these T cell-based immunotherapies have been difficult to implement because they require 4–6 weeks of manufacture, are costly, and have significant toxicities. This renewed interest in the potential of cellular immunity—and the manufacturing, supply chain, and administration logistics that have been addressed with these new agents—have ignited a new wave of enthusiasm for NK cell-directed therapies in NHL. With high safety profiles and proven anti-lymphoma efficacy, one or more new NK cell-directed modalities are certain to be introduced into the standard toolbox of NHL therapy within the next few years, be it function-enhancing cytokine muteins, multi-domain NK cell engagers, or adoptive therapy with expanded or genetically modified NK cells.

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Dissertations / Theses on the topic "NK cell therapy"

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Jaime-Ramirez, Alena Cristina. "HER2 and Folate Receptor Targeted Therapy is Enhanced by NK Cell-Activating Cytokines." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1364465780.

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Ojo, Evelyn. "Approaches to Improve the Proliferation and Activity of Natural Killer Cells for Adoptive Cell Therapy." Case Western Reserve University School of Graduate Studies / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=case1536760957918928.

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Wang, Siao-Yi. "Interactions between complement and cellular mediated mechanisms of monoclonal antibody therapy." Diss., University of Iowa, 2010. https://ir.uiowa.edu/etd/619.

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Monoclonal antibodies (mAbs) have become an important part of therapy for a number of cancers. The first mAb to be approved for clinical use is rituximab, which is currently used for the treatment of various B cell malignancies. Despite its clinical value, the mechanisms in which rituximab induces tumor regression are unclear. Growing evidence suggests that multiple mechanisms involving complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC) are involved. However, the direct interactions between CDC and ADCC have yet to be investigated. My studies examine the relationship between complement fixation and the activation of NK cells by utilizing in vitro assays, a syngeneic murine lymphoma model, and clinical samples from patients. Using these systems, I demonstrate that the initiation of the complement cascade inhibits NK cell activation and ADCC induced by rituximab in vitro. I also show that depletion of complement enhances the activation of NK cells and improves the efficacy of mAb therapy in a murine model. Lastly, I demonstrate that NK cell activation correlates with decreased complement activity in patients after rituximab treatment. The studies described in this dissertation have furthered the understanding of the mechanisms involved in antibody therapy. These results have described a novel inhibitory role for complement activity in the anti-tumor responses of mAbs. Furthermore, these findings suggest that strategies to circumvent the inhibitory effect of complement may improve how current mAbs are used and the how mAbs are designed in the future.

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Suck, Garnet, Yeh Ching Linn, and Torsten Tonn. "Natural Killer Cells for Therapy of Leukemia." Karger, 2016. https://tud.qucosa.de/id/qucosa%3A71644.

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Clinical application of natural killer (NK) cells against leukemia is an area of intense investigation. In human leukocyte antigen-mismatched allogeneic hematopoietic stem cell transplantations (HSCT), alloreactive NK cells exert powerful anti-leukemic activity in preventing relapse in the absence of graft-versus-host disease, particularly in acute myeloid leukemia patients. Adoptive transfer of donor NK cells post-HSCT or in non-transplant scenarios may be superior to the currently widely used unmanipulated donor lymphocyte infusion. This concept could be further improved through transfusion of activated NK cells. Significant progress has been made in good manufacturing practice (GMP)-compliant large-scale production of stimulated effectors. However, inherent limitations remain. These include differing yields and compositions of the end-product due to donor variability and inefficient means for cryopreservation. Moreover, the impact of the various novel activation strategies on NK cell biology and in vivo behavior are barely understood. In contrast, reproduction of the thirdparty NK-92 drug from a cryostored GMP-compliant master cell bank is straightforward and efficient. Safety for the application of this highly cytotoxic cell line was demonstrated in first clinical trials. This novel ‘off-theshelf’ product could become a treatment option for a broad patient population. For specific tumor targeting chimeric-antigen-receptor-engineered NK-92 cells have been designed.

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Ewen, Eva-Maria [Verfasser], and Viktor [Akademischer Betreuer] Umansky. "Pro-inflammatory cytokines unleash natural killer cell potential for tumor therapy : NK cells want to break free / Eva-Maria Ewen ; Betreuer: Viktor Umansky." Heidelberg : Universitätsbibliothek Heidelberg, 2019. http://d-nb.info/1180394402/34.

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RAMBALDI, BENEDETTA. "Understanding T and NK cell reconstitution after allogeneic hematopoietic cell transplantation: a path to improve graft versus leukemia and minimize graft versus host disease." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2023. https://hdl.handle.net/10281/402375.

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Il trapianto di cellule ematopoietiche (HCT) rappresenta una terapia cardine per il trattamento delle neoplasie ematologiche altrimenti incurabili. Tuttavia, la procedura di trapianto può essere gravata dalla recidiva della malattia, dalla malattia del trapianto contro l'ospite (GVHD) e dalle infezioni. Le cellule T e NK che ricostituiscono dopo l'HCT proteggono da infezioni e recidive, ma sono anche coinvolte nella patogenesi della GVHD. Gli obiettivi del mio progetto di dottorato erano di migliorare la comprensione della ricostituzione delle cellule T e NK, utilizzando campioni di donatori sani e pazienti dopo il trapianto e diversi approcci tecnici (citometria a flusso, citometria di massa, sequenziamento dell'RNA e test funzionale ex vivo) e sviluppare nuove strategie immunoterapiche basate sui linfociti T e NK dopo HCT. In primo luogo, abbiamo dimostrato che un ritardo nel recupero dei linfociti T, un rapporto Treg/Tcon più elevato, un'aumentata espressione di PD-1 sui linfociti T di memoria e un arricchimento di cellule NK a fenotipo immaturo sono stati osservati dopo HCT aploidentico (aplo-HCT) con l’utilizzo di ciclofosfamide post-trapianto. Inoltre, la funzione delle cellule NK CD56brightCD16+ immature funzionalmente alterate dopo aplo-HCT può essere migliorata con l’utilizzo dell'interleuchina-15 in vitro. In secondo luogo, abbiamo avviato uno studio di fase I sulle cellule cytokine-induced memory-like (CIML) NK infuse da donatore haploidentico in pazienti con neoplasie mieloidi che hanno avuto una recidiva dopo aplo-HCT. Nei primi 6 pazienti arruolati, l'infusione di cellule CIML-NK ha portato a una rapida espansione in vivo da 10 a 50 volte, che è stata mantenuta per mesi. L'infusione è stata ben tollerata, con febbre e pancitopenia come eventi avversi più comuni. Sulla base di questi dati preliminari, le cellule CIML-NK possono fungere da piattaforma per il trattamento della recidiva post-trapianto delle patologie mieloidi. Infine, ci siamo concentrati sul bilanciamento della risposta dei linfociti T per controllare l’incidenza di GVHD. CD6, un recettore co-stimolatorio dei linfociti T, che aiuta a stabilizzare la sinapsi immunologica tra la cellula T e l'APC, dopo legame con il suo ligando, la molecola di adesione delle cellule leucocitarie attivate (ALCAM). In questo contesto, il legame CD6-ALCAM promuove l'attivazione, la proliferazione e la maturazione delle cellule T. Abbiamo dimostrato che le cellule T CD6 ricostituivano subito dopo il trapianto, con le cellule Treg che esprimono livelli inferiori di CD6 rispetto alle cellule Tcon e cellule T CD8+. Dopo l'insorgenza della aGVHD, l'espressione sia di CD6 che di ALCAM è stata mantenuta. Itolizumab ha inibito l'attivazione e la proliferazione delle cellule T CD4+ e CD8+ nell'ambito di aGVHD in esperimenti ex vivo, senza mediare l'attività citolitica diretta o la citotossicità anticorpo-dipendente. I nostri risultati identificano la via di CD6-ALCAM come potenziale bersaglio per il controllo dell'aGVHD. Uno studio di fase I/II che utilizza itolizumab come trattamento di prima linea in combinazione con steroidi per i pazienti con aGVHD è attualmente in corso. In conclusione, questi risultati evidenziano la necessità di bilanciare le proprietà effettrici e tolerogeniche del sistema immunitario che si ricostituisce dopo HCT e suggeriscono differenti strategie per promuovere o moderare le funzioni delle cellule T e NK.
Hematopoietic cell transplantation (HCT) represents a cardinal therapy for hematological malignancy otherwise incurable. However, HCT can be complicated by disease recurrence, graft versus host disease (GVHD) and infections. After HCT, reconstituting T and NK cells protect against infection and relapse, but they are also involved in the pathogenesis of GVHD. The aims of my PhD project were to improve the understanding of T and NK-cell reconstitution, using samples from both healthy donor and patients after transplant and different technical approaches (flow cytometry, mass cytometry, RNA sequencing, and ex vivo functional assay) and to develop post-transplant T and NK cell-based immunotherapeutic strategies. First, we showed that delayed early T-cell recovery, a higher Treg/ Tcon ratio, an increased PD-1 expression on memory T cells, and an enriched immature NK phenotype were observed after haploidentical HCT (haplo-HCT) with post-transplant cyclophosphamide. In addition, the expansion of functionally impaired immature CD56brightCD16+ NK cells after haplo-HCT can be enhanced with in vitro interleukin-15 priming. Second, we initiated a phase I trial of adoptively transferred cytokine-induced memory-like (CIML) NK cells in patients with myeloid malignancies who relapsed after haplo-HCT. In the first 6 enrolled patients, infusion of CIML NK cells led to a rapid 10- to 50-fold in vivo expansion that was sustained over months. The infusion was well tolerated, with fever and pancytopenia as the most common adverse events. Based on these preliminary data, CIML NK cells may serve as a promising platform for the treatment of posttransplant relapse of myeloid disease. Finally, we focused on the balancing of T cell response to control GVHD occurrence. CD6, a pan-T cell co-stimulatory receptor, helps to stabilize the immunological synapse between the T cell and the APC, upon ligation, with its ligand, activated leukocyte cell adhesion molecule (ALCAM). In this context, CD6-ALCAM binding promotes T cell activation, proliferation, maturation. We showed that CD6 T cells reconstituted early after transplant with Treg expressing lower levels of CD6 compared to Tcon and CD8+ T cells. After onset of aGVHD, both CD6 and ALCAM expression was maintained. Itolizumab inhibited CD4+ and CD8+ T cell activation and proliferation in the setting of aGVHD in ex vivo experiments, without mediate direct cytolytic activity or antibody-dependent cytotoxicity. Our results identify the CD6-ALCAM pathway as a potential target for aGVHD control. A phase I/II study using itolizumab as first line treatment in combination with steroids for patients with aGVHD is currently ongoing. In conclusion, these results highlight the need of balancing the effector and tolerogenic properties of the immune system reconstituting after HCT and suggest different strategies to enhance or moderate the T and NK cells functions.

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Kübler, Ayline [Verfasser], and Rupert [Akademischer Betreuer] Handgretinger. "Optimization of NK cell-based immune therapy strategies against pediatric acute B cell precursor leukemia using a human-murine xenotransplantation model / Ayline Kübler ; Betreuer: Rupert Handgretinger." Tübingen : Universitätsbibliothek Tübingen, 2015. http://d-nb.info/1163664618/34.

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Craperi, Delphine. "Thérapie génique des gliomes : caractérisation des voies cytotoxiques déclenchées par le système thymidine kinase herpétique/ganciclovir." Université Joseph Fourier (Grenoble ; 1971-2015), 1998. http://www.theses.fr/1998GRE10073.

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La therapie genique par transfert du gene de la thymidine kinase du virus de l'herpes simplex de type 1 (hsv1-tk) suivi d'un traitement avec la prodrogue ganciclovir (gcv) a ete utilisee pour le traitement de divers cancers. L'efficacite de cette therapie est en partie due a l'existence d'un effet de toxicite de voisinage : le traitement au ganciclovir entraine non seulement la mort des cellules exprimant hsv1-tk mais aussi celle des cellules adjacentes non transfectees. Nous avons entrepris une etude in vitro des mecanismes moleculaires de la toxicite de ce systeme enzyme/prodrogue sur des lignees issues de tumeurs cerebrales. Les resultats obtenus montrent que le couple hsv1-tk/gcv declenche deux reactions cellulaires differentes au stress cytotoxique, selon les lignees utilisees. Dans un premier cas, le traitement au ganciclovir entraine un blocage du cycle cellulaire en phase s rapidement suivi d'une mort cellulaire associant des phenomenes d'apoptose et de necrose. Dans le second cas, le couple hsv1-tk/gcv declenche une mort cellulaire tardive et atypique, sans reel arret du cycle cellulaire. Ce phenomene, associe a l'apparition de cellules geantes et polyploides, est appele catastrophe mitotique et pourrait impliquer la proteine p21. Ces deux modes de mort cellulaire semblent independants de la proteine p53 et impliquent une activation de la proteine pro-apoptotique bax. Le gene represseur de la mort cellulaire bcl-2 inhibe en partie le processus apoptotique declenche par le systeme hsv1-tk/gcv ; ce gene pourrait donc jouer un role dans certaines formes de resistance observees au cours de cette etude. Ainsi, cette etude demontre que le phenotype tumoral va conditionner le destin cellulaire apres le traitement et s'avere donc un determinant critique de la sensibilite a cette approche therapeutique.

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GUOLO, FABIO. "POST-TRANSPLANT NIVOLUMAB PLUS UNSELECTED AUTOLOGOUS LYMPHOCYTES IN REFRACTORY HODGKIN LYMPHOMA PATIENTS: A SAFE AND EFFECTIVE THERAPY ASSOCIATED WITH EXPANSION AND MATURATION OF NK CELLS." Doctoral thesis, Università degli studi di Genova, 2021. http://hdl.handle.net/11567/1043790.

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Hodgkin Lymphoma (HL) is a B-Cell neoplasia with a favourable outcome in responding patients. However, despite the efficacy of first line therapy about 30% of patients eventually relapse or are refractory (R/R). Recently, the immune checkpoint inhibitor (CI) nivolumab demonstrated good activity in R/R HL patients although the complete response (CR) rate was less than 20%. The efficacy of nivolumab is strictly related to the host degree of immune competence, which is greatly impaired in heavily pre-treated HL patients after autologous stem cell transplantation (ASCT). To enhance the activity of CI, we explored the feasibility of the infusion of autologous lymphocytes (ALI) in combination with the pre-emptive administration of nivolumab, early post-ASCT, in patients affected by R/R HL. Eight patients (median age 29, range 18-56) with active R/R disease, who had already failed at least two chemotherapy lines and Brentuximab, were eligible for the trial. HL patients underwent early lymphocyte apheresis, with a target cell dose of 5x107 CD3+/kg. All patients then received ASCT with FEAM conditioning followed by ALI at a median time of 14 days after infusion, starting with 1x104 CD3+ cells/kg in the first infusion to a maximum of 1x107cells/kg in the fourth and last infusion. Each ALI was followed after 48 hours by the administration of nivolumab 240 mg flat dose. As a control cohort, two patients, in CR after second line chemotherapy, were given ALI only, without nivolumab. No grade 3 or 4 adverse events were recorded. All treated patients achieved negative PET scan after immunotherapy and are alive and disease-free after a median follow-up of 20 months. Two patients did receive allogeneic stem cell transplantation while in CR. Notably, compared to control patients, a faster expansion/reconstitution of highly differentiated NK cells was observed as well as a quicker T-cell recovery. These data suggest the potential role of PD-1 receptor in the direct or indirect control of NK cell maturation/development and, probably, NK anti-tumor activity. Thus, the combination of adoptive cell therapy with CI may represent a novel approach for chemorefractory HL patients.

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Oh, Jun Seok. "Critical Roles of Cytomegalovirus-Induced Natural Killer Cells in Chronic Hepatitis C Virus Infection and Rituximab-Mediated Cancer Therapy." Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/36228.

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Natural Killer (NK) cells, members of the innate lymphoid cells (ILCs), are known to play an important role in the defense against foreign cells and abnormal host cells that have arisen due to viral infection or cancer inducing mutations. The typical immune response of NK cells involves the release of cytotoxic granules containing perforin and granzyme, and the secretion of immune-regulatory cytokines such as interferon gamma (IFN-γ). Unlike the adaptive lymphocytes such as T cells and B cells, NK cells do not require prior sensitization, enabling them to initiate an immune response much faster. This unique feature of NK cells is made possible by the utilization of an array of germline encoded receptors; but on the other hand, it limits NK cells ability to respond against rapidly evolving pathogens. NK cells overcome this shortcoming with an antibody-assisted process called antibody dependent cellular cytotoxicity (ADCC). A novel subset of human NK cells, which displays potent and broad antiviral responsiveness in concert with virus-specific antibodies, was recently discovered in cytomegalovirus positive (CMV+) individuals. This NK cell subset, called g-NK cell, was characterized by a deficiency in the expression of FcεRIγ, an adaptor protein that associates with CD16 which enables ADCC. Surprisingly, despite this deficiency, g-NK cells displayed an enhanced ADCC as compared to their conventional counterparts. Furthermore, having a long-lasting memory-like NK-cell phenotype suggests a role for g-NK cells in chronic infections. This study investigates the importance of g-NK-cells in clinical settings, first by investigating whether the presence of g-NK cells is associated with the magnitude of liver disease during chronic hepatitis C virus (HCV) infection. Analysis of g-NK cell proportions and function in the peripheral blood mononuclear cells (PBMCs) of healthy controls and chronic HCV subjects showed that chronic HCV subjects had slightly lower proportions of g-NK cells, while having similarly enhanced ADCC responses compared to conventional NK cells. Notably, among CMV+ chronic HCV patients, lower levels of liver enzymes and fibrosis were found in those possessing g-NK cells. g-NK cells were predominant among the CD56neg NK cell population often found in chronic HCV patients, suggesting their involvement in the immune response against HCV. Rituximab is a chimeric anti-CD20 antibody used to treat B cell lymphoma patients; and studies have suggested that its efficacy is associated with the ADCC potency and CD16 affinity. Since g-NK cells are characterized by their superior ADCC compared to their conventional counterpart, I decided to investigate whether the presence of g-NK cells can improve the effectiveness of rituximab against malignant B cells in the context of lymphoma and leukemia. The analysis of g-NK cells’ ADCC response against rituximab-coated lymphoma cell lines and B cells from a CLL patient indicated a superior ADCC by g-NK cells compared to their conventional NK cell counterparts. Taken together, for the first time, my findings indicate that the presence of g-NK cells in CMV+ individuals is associated with milder liver disease in chronic HCV infection. In addition, an enhanced ADCC response by g-NK cells upon encountering rituximab coated target cells suggests the beneficial roles of g-NK cells, and opens an avenue for novel therapeutic approaches where g-NK cells can be utilized to treat persistent diseases such as chronic viral infection and cancer.

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Books on the topic "NK cell therapy"

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Schatt, Stephan. An animal model for in utero HSC transplantation and the role of cytokine secretion by T- and NK cells in pregnancy /von Stephan Schatt. Schatt, 2000.

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Book chapters on the topic "NK cell therapy"

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Lee, Dean Anthony, Laurence James Neil Cooper, and Elizabeth J. Shpall. "NK-Cell Immunotherapy for AML." In Targeted Therapy of Acute Myeloid Leukemia, 737–55. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1393-0_40.

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Henkart, Pierre A. "Mechanism of NK-cell mediated cytotoxicity." In Cancer Immunology: Innovative Approaches to Therapy, 123–50. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2629-8_4.

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Oguchi, Masahiko. "Extranodal NK/T Cell Lymphoma, Nasal Type." In Radiation Therapy for Extranodal Lymphomas, 29–37. Tokyo: Springer Japan, 2017. http://dx.doi.org/10.1007/978-4-431-56435-5_3.

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Li, Yexiong. "Extranodal NK/T-Cell Lymphoma, Nasal Type." In Radiation Therapy in Hematologic Malignancies, 157–80. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-42615-0_11.

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Lee, Dean Anthony, Laurence James Neil Cooper, and Elizabeth J. Shpall. "Erratum to: NK-Cell Immunotherapy for AML." In Targeted Therapy of Acute Myeloid Leukemia, E1. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-1393-0_44.

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Hu, Jinqiao. "CAR-NK Cell Therapy: A Promising Alternative to CAR-T Cell Therapy." In Proceedings of the 2022 6th International Seminar on Education, Management and Social Sciences (ISEMSS 2022), 372–81. Paris: Atlantis Press SARL, 2022. http://dx.doi.org/10.2991/978-2-494069-31-2_48.

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Nerina, Denaro, and Marco Carlo Merlano. "NK Cells in Immunotherapy: How Important Are They?" In Critical Issues in Head and Neck Oncology, 65–81. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63234-2_5.

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AbstractNK cells are able to perform multiple functions, ranging from immunosurveillance to elimination of mutated or damaged cells, through many different cytotoxic mechanisms. Their functions can be very useful for cancer immunotherapy. But to achieve the maximum support from these extraordinary cells it is necessary to know their effector mechanisms and the mechanisms that lead to their suppression. We have briefly summarized some interesting aspect of their role in immunosurveillance of cancer and metastases, the major mechanisms of cell cytotoxicity, in particular their role in antigen dependent cell cytotoxicity, and many promising strategies currently under study to improve the anticancer function of these cells.Finally, we have taken a closer look at cell therapy in this context, comparing CAR-NK cells and CAR-T cells showing the potential advantages of the former over the latter.

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Multhoff, G., E. A. Repasky, and Peter Vaupel. "Mild Hyperthermia Induced by Water-Filtered Infrared A Irradiation: A Potent Strategy to Foster Immune Recognition and Anti-Tumor Immune Responses in Superficial Cancers?" In Water-filtered Infrared A (wIRA) Irradiation, 129–39. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-92880-3_10.

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AbstractApart from a number of positive “physiological” effects such as an increase in local blood flow which results in an improved oxygen supply and a reversal of tumor hypoxia, a key hallmark of cancer growth which greatly impairs anti-tumor immune responses, hyperthermia (HT) also exerts beneficial effects on anti-cancer immunity. The water-filtered infrared A (wIRA) irradiation technique achieves tissue temperatures in the fever-range (tT = 39–41 °C) or mild hyperthermia levels (tT = 39–43 °C) up to tissue depths of ≈25 mm in tissues. At tissue temperatures of 39–43 °C, by fostering the reactivity of the “immunological” TME [e.g., the activity of CD8+ cytotoxic T cells, CD4+ helper T cells, dendritic cells (DC), M1 macrophages, natural killer (NK) cells, and NK-like T (NK-T) cells], while compromising immunosuppressive cells [e.g., tumor-associated M2 macrophages (TAMs), myeloid-derived suppressor cells (MDSCs), regulatory T (Treg) cells]. Moreover, elevated temperatures resulting in mild hyperthermia induce the synthesis and release of heat-shock proteins (HSPs), and thereby augment tumor antigenicity.

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Whiteside, T. L., N. L. Vujanovic, and R. B. Herberman. "Natural Killer Cells and Tumor Therapy." In Specificity, Function, and Development of NK Cells, 221–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-46859-9_13.

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Chu, Yaya, Allyson Flower, and Mitchell S. Cairo. "Modification of Expanded NK Cells with Chimeric Antigen Receptor mRNA for Adoptive Cellular Therapy." In Natural Killer Cells, 215–30. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3684-7_18.

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Conference papers on the topic "NK cell therapy"

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Cichocki, Frank, Barham Valamehr, Ryan Bjordahl, Bin Zhang, Dhifaf Sarhan, Sarah Cooley, Bruce Blazar, et al. "Abstract 3752: FATE-NK100: A novel NK cell-mediated cancer therapy." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3752.

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Korbelik, Mladen, and Jinghai Sun. "Cancer treatment by photodynamic therapy combined with NK-cell-line-based adoptive immunotherapy." In BiOS '98 International Biomedical Optics Symposium, edited by Steven L. Jacques. SPIE, 1998. http://dx.doi.org/10.1117/12.308148.

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Teng, Kun-Yu, Anthony Mansour, Zhu Zheng, Lei Tien, Yi Zheng, Zhiyao Li, Jianying Zhang, Saul J. Priceman, Michael A. Caligiuri, and Jianhua Yu. "Abstract LB154: A potent human CAR NK cell therapy directed against pancreatic cancer." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-lb154.

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Pellom, Samuel Troy, Anshu Malhotra, and Anil Shanker. "Abstract B107: Combination therapy of kidney cancer using bortezomib and natural killer (NK) cell transfer." In Abstracts: AACR International Conference on the Science of Cancer Health Disparities‐‐ Sep 18-Sep 21, 2011; Washington, DC. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1055-9965.disp-11-b107.

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Morales, Lucia, Sandra Pinto Nunes, Ester Munera-Maravilla, Jose Antonio Casado, Paula Río, Antonio Valeri, Edurne San José-Enériz, Xavier Agirre, Felipe Prosper, and Jesús María Paramio. "Abstract P064: Dual effect of epigenetic inhibitor and CAR-NK cell therapy in bladder cancer." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 5-6, 2021. American Association for Cancer Research, 2022. http://dx.doi.org/10.1158/2326-6074.tumimm21-p064.

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Seidel, Diana, Anastasia Shibina, C. Patrick Reynolds, Winfried S. Wels, Nicole Huebener, and Holger N. Lode. "Abstract 2808: GD2-specific genetically engineered NK cell therapy is effective in a drug-resistant neuroblastoma xenograft mouse model." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2808.

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Chung, Yong Yoon, Seung Woo Park, Jung-Min Im, Da-Kyung Yoo, Hyo-Cheon Cheon, Jae-Eun Kim, Kyeong-Pill Lim, et al. "Abstract CT171: Combinatorial allogeneic NK cell therapy with Pembrolizumab for cholangiocarcinoma; interim report of open label Phase1/2a study." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-ct171.

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Goulding, John, Bryan Hancock, Robert Blum, Wen-I. Yeh, Chia-Wei Chang, Mochtar Pribadi, Yijia Pan, et al. "204 Combining FT536, a pan-tumor targeting CAR NK cell therapy, with CD16 engagers provides a coordinated targeting strategy to overcome tumor heterogeneity." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0204.

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Razmara, Aryana, Lauren Farley, Rayna Harris, Sean Judge, Marshall Lammers, Cordelia Dunai, William Murphy, Robert Rebhun, Michael Kent, and Robert Canter. "272 Pre-clinical evaluation and first-in-dog clinical trials of intravenous infusion of PBMC-expanded adoptive NK cell therapy in dogs with cancer." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0272.

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Rogers, Paul, Bitna Yang, Hyojin Kim, Yusun Kim, Sunglim Cho, Bret Morin, Amanda Conerty, et al. "306 Evaluation of AB-101, an allogeneic cord blood-derived natural killer (NK) cell therapy, as an ADCC enhancer in hematologic and solid tumors." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0306.

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Reports on the topic "NK cell therapy"

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Kohrt, Holbrook. Augmenting Trastuzumab Therapy Against Breast Cancer Through Selective Activation of NK Cells. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada573699.

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Kohrt, Holbrook. Augmenting Trastuzumab Therapy Against Breast Cancer Through Selective Activation of NK Cells. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada595679.

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