Relevant bibliographies by topics / NK cell cytotoxicity assay

Academic literature on the topic 'NK cell cytotoxicity assay'

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Published: 18 August 2021
Last updated: 1 February 2022

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  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Journal articles on the topic "NK cell cytotoxicity assay":

1

Motzer, Sandra Adams, Joyce Tsuji, Vicky Hertig, Sandra K. Johnston, and James Scanlan. "Natural Killer Cell Cytotoxicity: A Methods Analysis of Versus Flow Cytometry Chromium Release." Biological Research For Nursing 5, no. 2 (October 2003): 142–52. http://dx.doi.org/10.1177/1099800403257196.

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The purpose of this study is to describe design considerations for the use of flow cytometry (FC) com-pared to51chromium (51Cr)-release assays utilizing cryopreserved peripheral blood mononuclear cells (PBMCs) to detect natural killer (NK) cell cytotoxicity. Subjects were 10 healthy women aged 18 to 39 years. Intra-assay variability between methods differed only at the lowest effector-target ratios evaluated. Interassay variability was wide but did not differ between methods. The relationship of lytic unit-10 between methods was strongly positive. Cytotoxicity detected by51Cr release was higher than that detected by FC for all 10 subjects. Cost was comparable. How-ever, had more assays been performed, technician time would have been greater with flow cytometry. More whole blood was needed to perform the flow cytometry cytotoxicity assay than51Cr-release cytotoxicity assay. The authors found no compelling reason to adopt NK cell cytotoxicity by flow cytometry over51Cr release.
2

Park, Ki-Hyun, Hyesun Park, Myungshin Kim, Yonggoo Kim, Kyungja Han, and Eun-Jee Oh. "Evaluation of NK Cell Function by Flowcytometric Measurement and Impedance Based Assay Using Real-Time Cell Electronic Sensing System." BioMed Research International 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/210726.

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Although real-time cell electronic sensing (RT-CES) system-based natural killer (NK) cytotoxicity has been introduced, it has not been evaluated using human blood samples. In present study, we measured flowcytometry based assay (FCA) and RT-CES based NK cytotoxicity and analyzed degranulation activity (CD107a) and cytokine production. In 98 healthy individuals, FCA with peripheral blood mononuclear cells (PBMCs) at effector to target (E/T) ratio of 32 revealed 46.5 ± 2.6% cytolysis of K562 cells, and 23.5 ± 1.1% of NK cells showed increased degranulation. In RT-CES system, adherent NIH3T3 target cells were resistant to basal killing by PBMC or NK cells. NK cell activation by adding IL-2 demonstrated real-time dynamic killing activity, and lymphokine-activated PBMC (E/T ratio of 32) from 15 individuals showed 59.1 ± 6.2% cytotoxicity results after 4 hours incubation in RT-CES system. However, there was no significant correlation between FCA and RT-CES cytotoxicity. After K562 target cell stimulation, PBMC produced profound proinflammatory and immunoregulatory cytokines/chemokines including IL-2, IL-8, IL-10, MIP-1αβ, IFN-γ, and TNF-α, and cytokine/chemokine secretion was related to flowcytometry-based NK cytotoxicity. These data suggest that RT-CES and FCA differ in sensitivity, applicability and providing information, and further investigations are necessary in variable clinical conditions.
3

Kim, Dong Hwan, Suzanne Kamel-Reid, Hong Chang, Robert Sutherland, Chul Won Jung, Hyeoung Joon Kim, Je-Jung Lee, and Jeffrey H. Lipton. "Natural Killer (NK) or NK/T Cell Lineage Large Granular Lymphocytosis Associated with Dasatinib Therapy for Philadelphia Chromosome Positive Leukemia." Blood 112, no. 11 (November 16, 2008): 933. http://dx.doi.org/10.1182/blood.v112.11.933.933.

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Abstract Dasatinib, a dual tyrosine kinase inhibitor, is known to modulate or suppress T-cell activation and proliferation. We report a series of patients of chronic peripheral lymphocytosis development, identified as natural killer (NK) cells or NK/T-cells based on their large granular lymphocyte (LGL) morphologies and CD16+CD56+CD3− or CD3+ immunophenotypic profiles during dasatinib therapy. All cases that developed LGL lymphocytosis achieved optimal molecular response (8/8 in LGL+ patients vs 3/10 in LGL− patients, p=0.002). A 51Cr release assay demonstrated that NK cell cytotoxicity has been enhanced in a case of LGL lymphocytosis compared to normal healthy donors (Figure 1), and that NK cell cytotoxicity in dasatinib-responders was superior to that in non-responders (Figure 2). In summary, the present study suggests that NK or NK/T cell lineage LGL lymphocytosis develops associated with dasatinib therapy and that LGL might have a therapeutic effect on Ph+ leukemic cells. Figure 1. Cytotoxicity of NK cells isolated from the patients developing large granular lymphocytosis following dasatinib therapy as assessed by 51Cr release assays using target cells as K562 (A) and T2 cell line (B) as target cells. Figure 1. Cytotoxicity of NK cells isolated from the patients developing large granular lymphocytosis following dasatinib therapy as assessed by 51Cr release assays using target cells as K562 (A) and T2 cell line (B) as target cells. Figure 2. The result of 51Cr release assays comparing cytotoxicity of NK cells isolated from patients responding to dasatinib therapy (responder) and not responding (non-responder) following dasatinib therapy using K562 cell line as target cells. Figure 2. The result of 51Cr release assays comparing cytotoxicity of NK cells isolated from patients responding to dasatinib therapy (responder) and not responding (non-responder) following dasatinib therapy using K562 cell line as target cells.
4

Ribeiro-Dias, Fátima, and Carlos Eduardo Tosta. "Dynamics and kinetics of natural killer cell cytotoxicity in human malaria as evaluated by a novel stepwise cytotoxicity assay." Revista da Sociedade Brasileira de Medicina Tropical 39, no. 4 (August 2006): 357–64. http://dx.doi.org/10.1590/s0037-86822006000400008.

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Malaria causes important functional alterations of the immune system, but several of them are poorly defined. To evaluate thoroughly the natural killer cell cytotoxicity in patients with malaria, we developed a technique capable to assess both the dynamics and the kinetics of the process. For the kinetics assay, human peripheral blood mononuclear cells were previously incubated with K562 cells and kept in agarose medium, while for the dynamics assay both cells were maintained in suspension. NK activity from patients with vivax malaria presented a kinetics profile faster than those with falciparum malaria. NK cytotoxicity positively correlated with parasitemia in falciparum malaria. The dynamics of NK cytotoxicity of healthy individuals was elevated at the beginning of the process and then significantly decreased. In contrast, malaria patients presented successive peaks of NK activity. Our results confirmed the occurrence of alteration in NK cell function during malaria, and added new data about the NK cytotoxicity process.
5

Lachota, Mieszko, Marta Siernicka, Zofia Pilch, Agnieszka Graczyk-Jarzynka, and Magdalena Winiarska. "Dasatinib Effect on NK Cells and Anti-Tumor Immunity." Blood 132, Supplement 1 (November 29, 2018): 3004. http://dx.doi.org/10.1182/blood-2018-99-111280.

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Abstract Introduction Dasatinib is a potent small molecule kinase inhibitor targeting BCR-ABL kinase - oncogenic driver in Philadelphia chromosome-positive (Ph+) cases of chronic myelogenous leukemia (CML). In addition to BCR-ABL kinase, it also targets a broad array of other kinases, affecting not only leukemia cells but also immune cells. Just one hour after dasatinib oral administration a rapid increase of NK, NKT, T and B cells is observed in peripheral blood. Dasatinib has been also shown to influence NK cell cytotoxicity, however, the results are discordant. Some groups observe potentiation of NK cell cytotoxic activity while others strong inhibitory effects. These inconsistencies may be explained by differences in in vitro protocols used to study this phenomenon. Aim Our study aims to investigate dasatinib influence on immune cells in whole blood assays resembling physiological conditions observed in patients. In particular, we want to investigate dasatinib effect on NK cell mobilization, degranulation, and anti-tumor immunity. In light of clinical and pre-clinical studies involving dasatinib and the importance of NK cells in cancer, it is crucial to establish the mechanisms and kinetics of dasatinib immunomodulatory activity. Methods Before and one hour after first dasatinib administration peripheral blood was collected from CML patients. Collected whole blood was directly added to the target K562 cell line. After co-incubation, erythrocytes were lysed, cells were stained with a panel of monoclonal antibodies and analyzed with flow cytometry. A relative increase in lymphocyte count was determined by Trucount Tubes (BD). Dasatinib effect on NK cells in vitro was studied with degranulation and cytotoxicity assays using NK cells isolated from healthy volunteers PBMCs. Dasatinib at clinically relevant concentrations (20-200mM) was used to assess its effect on NK cell degranulation, cytotoxicity, cytokine, and chemokine production with flow cytometry upon staining with anti-CD107a, TNF-α, IFN-γ and CCL-4 monoclonal antibodies. For in vivo experiments C57BL/6 mice were inoculated with EL4 tumor cell line stably expressing luciferase and human CD20. 3 days after tumor inoculation mice were treated with dasatinib or vehicle intraperitoneally (i.p.) in a dose of 30 mg/kg. To monitor tumor growth, mice were injected with luciferin and imaged using the IVIS system. Results In agreement with previous reports, we confirm NK, NKT, T and B cell count increase in peripheral blood after dasatinib administration. To evaluate how dasatinib influences NK cell cytokine and chemokine production we stimulated NK cells with K562 cell line. Production of major proinflammatory cytokines secreted by NK cells, TNF-α and IFN-γ, was inhibited by dasatinib treatment. Production of MIP-1β (CCL4), a chemokine secreted by NK cells attracting a broad spectrum of immune cells to inflammation sites, was also profoundly decreased. According to our findings, dasatinib presence during the cytotoxicity assay, in a dose-dependent manner, inhibits NK cell cytotoxicity. However, 24-hour dasatinib pretreatment increases their cytotoxic potential. To better mimic the physiological conditions we used whole blood degranulation assay which closely resembles patient settings, including dasatinib concentration. One hour after dasatinib intake we observed a potent inhibitory effect of dasatinib on NK cell degranulation. Additionally, we observed a shift in NK cell subpopulations - dasatinib present during degranulation assay decreases CD16⁻ NK cell number. Finally, we evaluated the influence of high-dose dasatinib treatment on tumor rejection in mice. Mice treated with dasatinib exhibit significantly increased tumor growth compared with vehicle-treated mice. Conclusions Using whole blood degranulation assay and in vitro degranulation and cytotoxicity assays we report that dasatinib effect on NK cell cytotoxicity is dose- and time-dependent. Our results indicate that dasatinib has a dual effect on NK cell degranulation and affects other NK cell functions including cytokine production and migration. Further studies are needed to evaluate the significance of these findings. Disclosures No relevant conflicts of interest to declare.
6

Smith, Katherine, Glenn Heller, and Peter Maslak. "Validation of Flow Cytometric Measurements of NK Cytotoxicity Against Chromium Release Assay for Use in Clinical Monitoring of Immune Function." Blood 108, no. 11 (November 16, 2006): 5287. http://dx.doi.org/10.1182/blood.v108.11.5287.5287.

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Abstract Chromium (51Cr) release assays have long been a standard technique for measuring the cytolytic activity of various immune effector cells. Although relatively easy to perform, these assays suffer from problems with sensitivity and require special radiation precautions limiting their routine use in clinical laboratories. Several flow cytometric techniques measuring cytotoxicity have been introduced and used as a measure of immune response. These assays are more rapid than the 51Cr based assay and have the added advantage of freeing the laboratory from the precautions required when working with radioactivity. Such testing has however largely been restricted to the research setting. In an attempt to extend these benefits to a clinical laboratory, we attempted to validate two commercially available flow cytometry kits (CyToxiLux Plus® & GranToxiLux®, OncoImmunin, Gathersburg, MD) measuring either caspase or granzyme B activity inside K562 target cells induced by interaction with NK cells. These assays were then compared with a standard NK cytotoxicity assay using 51Cr release technique. With K562 as a target, we parallel tested three CD56+CD3-KIR- NK clones; both the 51Cr and caspase based cytotoxicity values were highly positive. With WH autologous EBV cell line as target, we parallel tested five NK clones and five normal control donors as effectors. As expected, all cytotoxicity values for both assays were <10%. The caspase and granzyme assays were then compared and the degree of separation in the flow cytometric plots of the granzyme based assay were found to be marginally superior facilitating analysis of the data. The granzyme B assay therefore was chosen for investigation in the clinical samples. The granzyme and 51Cr assays were then compared both in 49 normal control donors and in 10 patients. There was a high level of concordance between the two assays. Comparing all results using linear correlation yielded a squared correlation (R2) value of 0.6878. However, given the wide range of NK activity in normal control donors the degree of positivity may not be clinically significant. Therefore, the data was examined in the context of a positive 51Cr response. Using a 2×2 table to exam the level of agreement, the kappa statistic was 0.63, indicating good agreement between the assays. When progressively fewer effector cells were added to a fixed number of target cells, the % cytotoxicity decreased from 39% to 0% with the flow cytometric assay and from 26% to 1% with the 51Cr assay. In the normal control donors the positive values ranged from 17% to 65% cytotoxicity using the flow assay compared with the previous range of 15% to 72% established with 51Cr. Patients having cytotoxicity values below 17% were deemed as having an unreactive or abnormal low result. One of the patients with few CD56+CD3- NK cells had consistently low cytotoxicity each time tested. For the patients who have either undergone allogeneic stem cell transplantation or have a known immunodeficiency, further clinical follow-up will serve to establish the clinical relevance of these measurements. These preliminary data suggest that the flow cytometric technique can be used in the clinical setting for immune monitoring.
7

Widowati, Wahyu, Diana Krisanti Jasaputra, Teresa Liliana Wargasetia, The Fransiska Eltania, Alya Mardhotillah Azizah, Mawar Subangkit, I. Nyoman Ehrich Lister, Chrismis Novalinda Ginting, Ermi Girsang, and Ahmad Faried. "Apoptotic Potential of Secretome from Interleukin-Induced Natural Killer Cells toward Breast Cancer Cell Line by Transwell Assay." HAYATI Journal of Biosciences 27, no. 3 (July 1, 2020): 186. http://dx.doi.org/10.4308/hjb.27.3.186.

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Breast cancer (BC) is the number one cause of deaths from cancer in women. Metastasis in BC is caused by immunosurveillance deficiency, including impairment of Natural Killer (NK) cell maturation, low NK activity, and decreasing cytotoxicity. This study was performed to improve activating receptors and cytotoxicity of NK cells using interleukin 15 (IL15) against BC cells. Human recombinant IL15 was used to induce NK cells. To evaluate the potential of IL15 in inducing NK cells, we measured the activating and inhibiting receptors (NKG2D, NKG2A), apoptotic potency of NK cells on BC cells (MCF7) using transwell assay. The IL15 inducer on the NK cell were measured NKG2D, NKG2A gene expression with quantitative polymerase chain reaction (qPCR), (GzmB) secretion using ELISA, apoptotic gene expression of MCF7 using qPCR. IL15 increased NKG2D expression 4.01-9.13%, but IL15 could not affect toward NKG2A expression on NK cells. IL15-activated NK cells, inhibited BC cells proliferation, induced apoptotic BC cells 25.89-32.19%, induced apoptotic genes of BC cells bax, p53. IL15 increase NK activating receptor (NKG2D), inhibit BC cells proliferation, induce apoptotic percentage and induce apoptotic gene expression.
8

Lundgren, T., R. S. Parhar, S. Renvert, and D. N. Tatakis. "Impaired Cytotoxicity in Papillon-Lefèvre Syndrome." Journal of Dental Research 84, no. 5 (May 2005): 414–17. http://dx.doi.org/10.1177/154405910508400503.

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Papillon-Lefèvre syndrome (PLS), palmoplantar hyperkeratosis with periodontitis, has been genetically characterized. However, suspected associated immune dysfunctions remain elusive. The purpose of this study was to evaluate peripheral blood lymphocyte levels and natural killer (NK) cell cytotoxicity in PLS. Twenty patients and 20 healthy controls were examined. Peripheral blood lymphocytes were analyzed by flow cytometry for surface markers. NK cell cytotoxicity against K562 cells was determined by means of a 51Cr release assay. White blood cell differential and proportions of B-, T-, T-helper, T-suppressor, and NK cells revealed only sporadic borderline variations from control values. In contrast, NK cell cytotoxicity was consistently and severely depressed (32–53% of control values) in all patients. To the best of our knowledge, this newly described impairment of NK cell cytotoxic function is the first consistent immune dysfunction reported in PLS. This suggests that the impaired NK cell cytotoxicity might contribute to the pathogenesis of PLS-associated periodontitis.
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Yurdakul Mesutoglu, Pinar, Hasan Yalim Akin, Merve Bunsuz, Eylul Turasan, Mustafa Merter, Cemalettin Ozturk, Klara Dalva, and Meral Beksac. "KIR 2DS4 May Influence Autologous and Cord Blood(CB) Natural Killer (NK)Cell Mediated in Vitro Cytotoxicity Against Freshly Isolated Human Bone Marrow Myeloma Plasma Cells and Cell Lines." Blood 132, Supplement 1 (November 29, 2018): 1920. http://dx.doi.org/10.1182/blood-2018-99-112837.

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Abstract Background and Aim: NK cell effects are mediated by Killer Immunoglobulin-like Receptor (KIR) inhibition. There are few reports on the protective role of KIRs against relapse in myeloma(MM) (Gabriel et al Blood 2010, Kröger et al leukemia 2011). However, which NK cells or for whom will be more effective and the role of individual differences in this mechanism is indefinite. In this study we aimed to accomplish cytotoxicity against both MM cells and human myeloma cell lines (HMCL) and to compare the cytotoxicity achieved with CB versus autologous NK cells as well as to investigate the influence of NK cell KIR geno/phenotypes. Patients and Methods: A total of 18 patients with refractory/relapsed MM were included in this study. Cell culturing: CD138+ PC isolated from fresh bone marrow aspirates of relapsed MM patients or HMCL (U266, RPMI8226 and H929) using RosetteSep™ Human Multiple Myeloma Cell Enrichment Cocktail (StemCell Technologies) were subjected to cytotoxicity assays with CB derived or autologous PB derived NK cells expanded in the presence of IL-15 (10ng/ml) for 2-8 days. Phenotyping: Effector cells (autologous or CB-NK) were analyzed by flow cytometry using CD45, CD3, CD16, CD56, CD158a (KIR2DL1), CD158i (KIR2DS4) and CD158b1/b2 (KIR 2DL2/2DL3) monoclonal antibodies. Cytotoxicity assays: 3,3 dioctadecyloxacarbocyanine perchlorate (DiO) dye was used to distinguish target cells (PC) from effector cells (NK). PC and NK cells were mixed at an 1:10 target: effector cell ratio and inoculated with Propidium Iodide (PI) in order to counter stain the dead cells. Naive PC were used as controls. Following 120 mins of incubation, PC death was evaluated using flow cytometry. After incubation of target cells (PC) with effector cells (NK cells), cytotoxic effects were determined by subtraction of NK mediated PC death from spontaneous PC death. Results: Following IL-15 expansion NK cells were found to express the CD16+56+3- phenotype. Eighteen MM patient PCs and six different HMCL samples were used in cytotoxicity assays(Table 1). In vitro PC viability was less than 45% in four samples and could not be analyzed in the study. Following incubation of PC wo NK cells, spontaneous PC death ratio was found to be 22.6% (min-max: 3%-42.3%). Twelve cytotoxicity assays targeting six MM PC were performed with autologous and CB-derived NK cells. Autologous NK and CB NK mediated cytotoxicity median rates were found to be 19.0% (range: 1.4% - 43.6%) and 31.3% (range: 2.4% - 51.2%), respectively. Additionally, CB-NK cells were evaluated against HMCL samples (four U266, one RPMI8226 and one H929). Median cytotoxicity against HMCL was 27.4% (range: 5.6% - 52.1%). Highest cytotoxicity against MM PC (MM-9) and HMCL (H929) were achieved by CB NK cells (51.2% and 52.1 % respectively). There was no cytotoxic effect against PCs of patients MM6 and MM10 (Figure 1-2). Flow-cytometric phenotyping of effector NK cells showed consistency (10/13) with genotypes. Since only one (CB19) with 19% CD158i positivity was PCR negative, a %20 cut-off rate was chosen. Both CD158a (KIR2DL1) and CD158b1/b2 (KIR 2DL2/2DL3) were positive among all patients and no significant correlation with cytotoxic effects was detectable. However out of five high cytotoxic reactions three NK cells were 2DS4 (+). While out of eight assays which resulted with low cytotoxicity only three NK cells were positive for the activating KIR 2DS4. When we analyzed CB NK cells against HMCL U266, three CB NK cells two of which were 2DS4(+) showed high cytotoxicity, while the 2DS4(-) CB NKs did not. The only assay targeting RPMI-8226 which is known to be a NK resistant HMCL, KIR2DS4(+) (CB17) derived NK cells were not sufficiently cytotoxic. Conclusion: Allogeneic CB NK cells were able to induce higher cell kill than autologous PB-derived NK cells. KIR types of autologous NK cells were not predictive for cytotoxic efficacy. Lacking KIR2DS4 in CB NK cells was correlated with less cytotoxicity. Additionally, KIR2DS4(+) CB NK cells were found to be highly cytotoxic against both PC and HMCL. NK cells may be an effective alternative due to its profound clinical advantages such as matching for HLA or KIR ligand is not required. Furthermore, if confirmed by others, certain KIR haplotypes (ie Haplotype A and KIR2DS4 +) may offer better therapeutic potential. Acknowledgment: The study has been supported by Scientific and Research Council of Turkey (TUBITAK grant no: 115S579) and Turkish Academy of Sciences. Disclosures Beksac: Takeda: Membership on an entity's Board of Directors or advisory committees; Amgen,Janssen-Cilag,Celgene: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau.
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Won, S. J., and M. T. Lin. "Thermal stresses reduce natural killer cell cytotoxicity." Journal of Applied Physiology 79, no. 3 (September 1, 1995): 732–37. http://dx.doi.org/10.1152/jappl.1995.79.3.732.

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The effects of different ambient temperatures (Ta) on the splenic natural killer (NK) cell activity, effector-target cell conjugation activity, and NK cell numbers were assessed in male inbred C3H/HeNCrj mice (7–10 wk old). The splenic NK cytotoxic activities were examined in a 4-h 51Cr release assay in mouse spleen cells that were obtained 1, 2, 4, 8, or 16 days after exposure to Ta of 22, 4, or 35 degrees C. The percentage of conjugating lymphocytes was calculated by counting the number of single lymphocytes bound to single target cells per 400 effector cells. The numbers of NK cells were expressed by the percentage of 5E6-positive cells. The 5E6 identifies only a subset of NK cells. It was found that the splenic NK cell activity, the effector-target cell conjugation activity, or the NK cell number began to fall 1 day after cold (Ta 4 degrees C) or heat (Ta 35 degrees C) stress. After a 16-day period of either cold or heat exposure, the fall in the splenic NK cell activity, the effector-target cell conjugation activity, or the number of 5E6-positive subsets of NK cells was still evident. Compared with those of the control group (Ta 22 degrees C), the cold-stressed mice had higher adrenal cortisol concentration and lower colonic temperature, whereas the heat-stressed animals had higher adrenal cortisol concentration and higher colonic temperature during a 16-day period of thermal exposure. However, neither cold nor heat stress affected both the body weight gain and the spleen weight in our mice.
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Journal articles Dissertations / Theses

Dissertations / Theses on the topic "NK cell cytotoxicity assay":

1

Cortés-Kaplan, Serena. "A Small Molecule Drug Screening Identifies the Antibiotic Colistin Sulfate as an Enhancer of NK Cell Cytotoxicity." Thesis, Université d'Ottawa / University of Ottawa, 2021. http://hdl.handle.net/10393/42547.

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Cancer immunotherapy is an encompassing term referring to therapeutic strategies that aim to boost the immune system to fight cancer. These strategies include administering immune cells that have been altered to have greater anti-tumor activity or using biologics and small molecules that target immune components to also promote tumor clearance. Natural Killer (NK) cells are cells of the innate immune system that recognize and kill abnormal cells such as cancer cells and play an important role in the anti-tumor response. Because of their crucial role in tumor immunity, NK cells are prime targets for immunotherapies. Repurposing small molecule drugs is an attractive strategy to identify new immunotherapies from already approved drugs. Here, we screened 1,200 approved drugs from the Prestwick Chemical Library to identify drugs that increase NK cell cytotoxicity. We used a high-throughput luciferase-release cytotoxicity assay to measure the killing of the myeloid leukemia cell line, K562 cells expressing nano luciferase (NL) by NK92 cells, a human NK cell line. From the drug candidates identified from the screening assay, the antibiotic colistin sulfate increased cytotoxicity of the NK92 cell line and unstimulated human NK cells towards K562-NL cells. This increase in NK cytotoxicity was short-lived as pre-treating NK92 cells with colistin for 1 hour or 24 hours did not increase cytotoxicity. Also, we show pre-treating K562-NL target cells with colistin does not sensitize them to NK-mediated killing. Further studies are needed to uncover the mechanism of action of colistin, thus contributing to knowledge of fundamental NK cell biology regarding NK cell cytotoxicity which will aid in identifying additional small molecule drugs that enhance NK cell activity.
2

Husain, Ralf. "Hat die Belastung gestillter Kinder mit persistenten organischen Schadstoffen Einfluss auf natürliche Killerzellen?" Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2004. http://dx.doi.org/10.18452/15045.

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Gestillte Kinder sind über die Muttermilch mit persistenten organischen Schadstoffen (POPs) belastet. Tierexperimentelle Studien deuten auf eine besondere Empfindlichkeit des sich entwickelnden Immunsystems für POPs hin. Mögliche Effekte dieser Verbindungen auf den kindlichen Organismus sind bisher kaum untersucht. Es wurden potenzielle Einflüsse verschiedener POPs (PCDDs, PCDFs, PCBs, beta-HCH, HCB und pp-DDE) auf natürliche Killerzellen (NK-Zellen) und NK-Aktivität bei gestillten im Vergleich zu nicht gestillten Kindern untersucht. NK-Zellen sind eine Lymphozytensubpopulation (CD3-CD56/16+), die über ihre zytotoxische Aktivität allogene, virusinfizierte und maligne Zellen ohne vorherige Sensibilisierung töten kann. Es wurden 66 gesunde Kinder im Alter von 11-12 Monaten untersucht, davon waren 50 Kinder mindestens 4 Monate lang voll gestillt und 16 Kinder nicht gestillt. Aus einer Region mit bekannter erhöhter PCDD/PCDF-Belastung stammten 13 gestillte Kinder. Die NK-Zellzahlen wurden mittels Immunphänotypisierung am Durchflusszytometer bestimmt. Die Aktivität der NK-Zellen wurde mit einem nicht-radioaktiven, durchflusszytometrischen Zytotoxizitäts-Assay gemessen. Die POP-Konzentrationen im Blutfett der Probanden wurden kommerziell bestimmt. Weder bei den NK-Zellzahlen, noch bei der NK-Aktivität konnten zwischen den gestillten und nicht-gestillten Kindern signifikante Unterschiede im t-Test nachgewiesen werden. In Korrelationsanalysen zeigten sich keine signifikanten Einflüsse der POP-Konzentrationen auf NK-Zellzahlen und NK-Aktivität. Im Laufe der Untersuchung zeigte sich, dass der eingesetzte Zytotoxizitäts-Assay nur semiquantitative Daten lieferte. Die vorliegenden Ergebnisse und weitere Befunde bezüglich des Immunsystems der Probanden weisen darauf hin, dass die relativ hohe Belastung lange gestillter Säuglinge mit POPs nicht zu einer biologischen Wirkung im kindlichen Organismus führt. Angesichts der nachgewiesenen positiven Effekte des Stillens, kann diesbezüglich die bestehende Stillempfehlung bekräftigt werden.
Breast-fed infants are exposed to persistent organic pollutants (POPs) via breast milk. Animal studies indicate a special sensitivity of the maturing immune system to POPs. Possible effects of these compounds on the infantile organism are so far barely examined. Potential influences of several POPs (PCDDs, PCDFs, PCBs, beta-HCH, HCB and pp-DDE) on natural killer (NK) cells and NK activity of breast-fed infants in comparison to formula-fed infants were investigated. NK cells are a subset of lymphocytes (CD3-CD56/16+) that can kill allogeneic, virus-infected and malignant cells via their cytotoxic activity without prior sensitization. The study group consisted of 66 healthy infants examined at age 11 to 12 months, of which 50 infants were breast-fed and 16 infants were formula-fed. 13 breast-fed infants came from a region with known increased PCDD/PCDF-burden. Numbers of NK cells were measured by flow cytometric immunophenotyping. NK activity was analysed by a non-radioactive flow cytometric cytotoxicity assay. POP concentrations in the blood fat of the probands were calculated commercially. There were no significant differences between breast-fed and formula-fed infants concerning number and activity of NK cells in the t-test. Analysis of correlation showed no significant influences of POP concentrations on the number and activity of NK cells. In the course of the study the data obtained by the employed cytotoxicity assay proved to be only semiquantitative. The presented findings and further results concerning the immune system of the study subjects suggest that the relatively high burden of long-term breast-fed infants with POPs does not lead to a biological effect in the infantile organism. Regarding the proven positive effects of breast-feeding the existing recommendation to breastfeed can be encouraged.
3

Chan, Gordon. "The role of Vav-1, Vav-2 and Lsc in NK T-cell development and NK cell cytotoxicity." Doctoral thesis, [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=966206258.

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Wallin, Robert. "Early induced immune responses : regulation of dendritic cell and NK cell functions /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-738-x.

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Huang, Anfei [Verfasser]. "Progranulin Prevents Regulatory NK Cell Cytotoxicity Against Antiviral T Cells / Anfei Huang." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2021. http://d-nb.info/123423341X/34.

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Carlsten, Mattias. "Molecular specificities of NK cell-mediated recognition of human tumor cells." Stockholm, 2010. http://diss.kib.ki.se/2010/978-91-7409-686-6/.

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Toomey, Jennifer. "The recognition of MHC Class I molecules by foetal NK cells." Thesis, University of Newcastle Upon Tyne, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310128.

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Srpan, Katja. "Regulation of Natural Killer cell cytotoxicity by shedding of the Fc receptor CD16." Thesis, University of Manchester, 2018. https://www.research.manchester.ac.uk/portal/en/theses/regulation-of-natural-killer-cell-cytotoxicity-by-shedding-of-the-fc-receptor-cd16(8bafd31a-ee93-4e46-ae0e-c6781bbeda79).html.

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Abstract:
Natural Killer (NK) cells are cytotoxic lymphocytes that can recognize and kill virally infected or tumour transformed cells by the secretion of cytolytic granules containing perforin. An individual NK cell can kill several target cells sequentially. Each target cell can trigger NK cell activation via different activating ligands and here we report that the order in which ligands are encountered affects the NK cell response. When NK cells are repeatedly activated via their Fc receptor CD16, with the therapeutic antibody rituximab, perforin secretion decreases with each stimulation. However, perforin secretion is restored to its initial level upon subsequent activation by MICA, which ligates NKG2D. Repeated stimulation of NK cells via MICA also decreases the degranulation capacity of NK cells but, strikingly, this effect cannot be rescued by a subsequent stimulation with rituximab. The strength of perforin secretion is also translated to killing of Daudi target cells, expressing different ligands. When Daudi, opsonised with rituximab is the first target NK cell encounters, the sequential killing of another opsonised rituximab or Daudi, expressing MICA will not be affected. But, when Daudi-MICA is met first, the consecutive killing of Daudi-MICA as well as Daudi-rituximab will be impaired. We found that the mechanism underlying these differential outcomes involves shedding of CD16, which occurs upon NK cell activation through both, CD16 and NKG2D. Shedding of CD16 renders the cells insensitive to further activation via that receptor but they remain competent for further activation through NKG2D. Interestingly, however, we also identified the beneficial role of CD16 shedding for NK cell serial killing. NK cells are more motile on rituximab-coated surfaces than on MICA-coated surfaces and their migration speed decreases upon inhibition of CD16 shedding. Moreover, the inhibition of CD16 shedding also prevents the NK cell detachment from rituximab opsonised Daudi cells. Thus, the shedding of the receptor can serve to augment NK cell motility to move between target cells. Efficient NK cell detachment also correlated with their increased survival. Finally, we report that CD16 is constitutively organised in small, dense nanoclusters and that the ligation with rituximab does not affect their spatial distribution. Despite the shedding of the receptor, leading to less protein molecules at the surface, the area of these clusters remains the same. Together these data suggest that CD16 shedding hinders NK cell cytotoxicity against opsonised targets, but promotes their movements between different targets. Thus, receptor shedding is important for efficient NK cell serial killing. Manipulation of CD16 shedding, perhaps by boosting its recovery, might therefore represent an important target for NK cell-based therapies including treatments with therapeutic antibodies.
9

Shibina, Anastasia [Verfasser]. "Fenretinide sensitizes multidrug-resistant human neuroblastoma cells to antibody-independent and ch14.18-mediated NK cell cytotoxicity / Anastasia Shibina." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2012. http://d-nb.info/103048760X/34.

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Jarrett, John M. "Synthesis and In-Vitro Cell Viability/Cytotoxicity Studies of Novel Pyrrolobenzodiazepine Derivatives." Digital Commons @ East Tennessee State University, 2017. https://dc.etsu.edu/honors/361.

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Abstract:
Pyrrolobenzodiazepines (PBDs) are a group of naturally occurring compounds that were discovered in the cultures of Streptomyces in the 1960s. Some natural PBDs discovered in these cultures, such as anthramycin and sibiromycin, were shown to possess a broad spectrum of anti-tumor activity. Since cancer is still a leading cause of death globally, the development of novel anti-proliferative derivatives of PBDs is essential for human welfare worldwide. Further synthesis and structure-activity relationship (SAR) studies of the parent natural products and their tetracyclic analogs will lead to the discovery of drug candidates. In this work, thirteen PBD analogues were synthesized using no more than three to four synthetic steps, beginning with commercially obtainable L-proline and isatoic anhydride. The MTT assay, which is a colorimetric assay that uses 3-(4,5-Dimethylthiazol-2-Yl)-2,5-diphenyltetrazolium bromide (MTT) to assess cell metabolic activity, was initially implimented to test the in vitro cytotoxicity of the compounds using multiple cell lines, namely: SKBR-3, MCF-7, SKMEL-2, CaCo 2, HCT 116, and Mia Paca. Nearly all of the compounds decreased the cell viability of MCF-7 by roughly 20%. Additionally, the anti-proliferative activity of the PBD products were further evaluated by the NCI-60 Human Tumor Cell Lines Screen, which is a part of the National Cancer Institute’s Development Therapeutics Program - Drug Synthesis and Chemistry Branch.
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Books on the topic "NK cell cytotoxicity assay":

1

Penner, Mark Douglas. NK cell mediated cellular cytotoxicity in C57BL/6 mice transgenic for antisene natural killer cell tumour recognition molecule p150. Ottawa: National Library of Canada, 1993.

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2

Lotzova, Eva. Nk Cell Mediated Cytotoxicity: Receptors, Signaling, and Mechanisms. CRC, 1992.

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3

1936-, Lotzová Eva, and Herberman Ronald B. 1940-, eds. NK cell mediated cytotoxicity: Receptors, signaling, and mechanisms. Boca Raton: CRC Press, 1992.

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1940-, Herberman Ronald B., Callewaert Denis M, and International Workshop on NK Cells (3rd : 1984 : Oakland University), eds. Mechanisms of cytotoxicity by NK cells. Orlando: Academic Press, 1985.

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B, Herberman Ronald, Callewaert Denis M, and International Workshop on NK Cells, (3rd : 1984 : Rochester), eds. Mechanisms of cytotoxicity by NK cells: Based on the Third International Workshop on NK Cells held at Meadow Brook Hall, Oakland University, Rochester, Michigan in May 1984. Orlando: Academic Press, 1985.

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Book chapters on the topic "NK cell cytotoxicity assay":

1

Aicheler, Rebecca J., and Richard J. Stanton. "Functional NK Cell Cytotoxicity Assays Against Virus Infected Cells." In Methods in Molecular Biology, 275–87. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-601-6_20.

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Aicheler, Rebecca J., and Richard J. Stanton. "Erratum To: Chapter 20 Functional NK Cell Cytotoxicity Assays Against Virus Infected Cells." In Methods in Molecular Biology, E1—E2. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-601-6_26.

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Lorenzo-Herrero, Seila, Christian Sordo-Bahamonde, Segundo González, and Alejandro López-Soto. "A Flow Cytometric NK Cell-Mediated Cytotoxicity Assay to Evaluate Anticancer Immune Responses In Vitro." In Methods in Molecular Biology, 131–39. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8885-3_8.

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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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Nishimoto, Fukiko, and Shiro Yamashoji. "A Rapid Cytotoxicity Assay of Metabolic Inhibitors." In Animal Cell Technology: Developments Towards the 21st Century, 1061–65. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0437-1_168.

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Chambers, B. J., J. L. Wilson, M. Salcedo, K. Markovic, M. T. Bejarano, and H. G. Ljunggren. "Triggering of Natural Killer Cell Mediated Cytotoxicity by Costimulatory Molecules." In Specificity, Function, and Development of NK Cells, 53–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-46859-9_5.

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Barrier, Marianne, Kelly Chandler, Susan Jeffay, Maria Hoopes, Tom Knudsen, and Sid Hunter. "Mouse Embryonic Stem Cell Adherent Cell Differentiation and Cytotoxicity Assay." In Methods in Molecular Biology, 181–95. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-867-2_11.

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Saudemont, Aurore, Shannon Burke, and Francesco Colucci. "A Simple Method to Measure NK Cell Cytotoxicity In Vivo." In Methods in Molecular Biology, 325–34. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-362-6_22.

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van der Haar Àvila, Irene, Patricia Marmol, Rolf Kiessling, and Yago Pico de Coaña. "Evaluating Antibody-Dependent Cell-Mediated Cytotoxicity by Chromium Release Assay." In Methods in Molecular Biology, 167–79. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8979-9_12.

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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.

Conference papers on the topic "NK cell cytotoxicity assay":

1

Sundararaman, Srividya, Kinga Karacsony, Diana Roen, Jaya Ghosh, and Paul V. Lehmann. "Abstract B57: NK cell-mediated cytotoxicity detection can be miniaturized by direct imaging in assay wells using a Terasaki plate format using only 100,000 effector cells (PBMC)." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-b57.

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Lovchik, Julie, and Mark Carter. "Abstract 1856: Donor and antibody diversity in NK cell-mediated antibody dependent cellular cytotoxicity (ADCC) detected using an optimized multiplexed assay and advanced flow cytometry." 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.am2021-1856.

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Tam, Kenric, Yunqin Lee, David Schoppy, and John B. Sunwoo. "Abstract 33: CEACAM1 blockade increases NK cell cytotoxicity in head and neck squamous cell carcinoma." In Abstracts: AACR-AHNS Head and Neck Cancer Conference: Optimizing Survival and Quality of Life through Basic, Clinical, and Translational Research; April 23-25, 2017; San Diego, CA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1557-3265.aacrahns17-33.

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Morton, Laura T., Anne K. Wouters, Dennis F. Remst, Renate S. Hagedoorn, Marleen M. Van Loenen, Renate de Boer, J. H. F. Falkenberg, and Mirjam H. M. Heemskerk. "Abstract A038: Effective rerouting of NK cell cytotoxicity against B-cell malignancies upon TCR gene transfer." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-a038.

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MacFarlane, Alexander, Tetyana Bagnyukva, Jiping Zhang, Kerry Campbell, Barry Jones, William Bachovchin, and Hossein Borghaei. "Abstract 2537: Antibody dependent cytotoxicity is enhanced by Ari-4175 through NK cell activation." 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.am2014-2537.

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Pangjaya, Lady Feren, Sanya Khaerunnisa, Nuzli Fahdia Mazfufah, Retno Lestari Budiman, and Radiana Dhewayani Antarianto. "Investigating different type of ovary cancer cell line for NK cell in vitro co-culture cytotoxic assay." In THE 5TH BIOMEDICAL ENGINEERING’S RECENT PROGRESS IN BIOMATERIALS, DRUGS DEVELOPMENT, AND MEDICAL DEVICES: Proceedings of the 5th International Symposium of Biomedical Engineering (ISBE) 2020. AIP Publishing, 2021. http://dx.doi.org/10.1063/5.0049155.

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Mayes, Kimberly, Zeinab Elsayed, Aiman Alhazmi, Michael Waters, Suehyb Alkhatib, Mark Roberts, Carolyn Song, et al. "Abstract A28: Tumor cell intrinsic BPTF inhibits NK cell activity and the abundance of natural cytotoxicity receptor co-ligands." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 1-4, 2017; Boston, MA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/2326-6074.tumimm17-a28.

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Ayuso, Jose Maria, Regan Truttschel, Max M. Gong, Mouhita Humayun, Amani Gillette, Manish Patankar, Melissa C. Skala, and David J. Beebe. "Abstract B32: Microfluidics to study solid tumor-NK cell interactions: From migration and cytotoxicity to therapeutic antibodies." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 1-4, 2017; Boston, MA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/2326-6074.tumimm17-b32.

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Truxova, Iva, Lenka Kasikova, Cyril Salek, Michal Hensler, Daniel Lysak, Peter Holicek, Pavla Bilkova, et al. "Abstract B96: Calreticulin exposure on malignant blasts correlates with improved NK cell-mediated cytotoxicity in AML patients." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-b96.

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Pellegatta, Serena, Gabriele Cantini, Sara Pessina, and Gaetano Finocchiaro. "Abstract A60: NK cell activation and cytotoxicity can be enhanced with chemotherapy in a murine model of glioblastoma." In Abstracts: AACR Special Conference on Tumor Immunology: Multidisciplinary Science Driving Basic and Clinical Advances; December 2-5, 2012; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tumimm2012-a60.

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