Relevant bibliographies by topics / Killer cells

Academic literature on the topic 'Killer cells'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Killer cells"

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WOODS, D. R., I. W. ROSS, and D. A. HENDRY. "A New Killer Factor Produced by a Killer/Sensitive Yeast Strain." Microbiology 81, no. 2 (February 1, 2000): 285–89. http://dx.doi.org/10.1099/00221287-81-2-285.

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Summary: The isolation of a new killer/sensitive phenotype of the yeast, Saccharomyces cerevisiae, is described. Killer/sensitive yeast cells are killed by the killer factor (KF1) secreted by killer yeast cells. The killer/sensitive cells also secrete a new killer factor (KF2) which kills sensitive cells. The production of KF2 by killer/sensitive cells renders them less sensitive to KF1, than sensitive cells. Sensitive cells are most susceptible to the action of KF2 in log phase. KF2 is a thermostable protein-containing killer factor.
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Abramova, V. A., A. Kali, N. Abdolla, O. Yu Yurikova, Yu V. Perfilyeva, Ye O. Ostapchuk, R. T. Tleulieva, S. K. Madenova, and N. N. Belyaev. "Influence of tumor cells on natural killer cell phenotype and cytotoxicity." International Journal of Biology and Chemistry 8, no. 1 (2015): 9–14. http://dx.doi.org/10.26577/2218-7979-2015-8-1-9-14.

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Mueller, K. L. "Killer Cells for Killer Bacteria." Science 333, no. 6051 (September 29, 2011): 1803. http://dx.doi.org/10.1126/science.333.6051.1803-b.

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Seaman, William E. "Natural killer cells and natural killer T cells." Arthritis & Rheumatism 43, no. 6 (June 2000): 1204–17. http://dx.doi.org/10.1002/1529-0131(200006)43:6<1204::aid-anr3>3.0.co;2-i.

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Perussia, Bice. "Lymphokine-activated killer cells, natural killer cells and cytokines." Current Opinion in Immunology 3, no. 1 (January 1991): 49–55. http://dx.doi.org/10.1016/0952-7915(91)90076-d.

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Kay, Neil E. "Natural Killer Cells." CRC Critical Reviews in Clinical Laboratory Sciences 22, no. 4 (January 1985): 343–59. http://dx.doi.org/10.3109/10408368509165790.

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Herberman, R. B. "Natural Killer Cells." Annual Review of Medicine 37, no. 1 (February 1986): 347–52. http://dx.doi.org/10.1146/annurev.me.37.020186.002023.

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Bevan, Michael J. "Stimulating killer cells." Nature 342, no. 6249 (November 1989): 478–79. http://dx.doi.org/10.1038/342478a0.

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Gardiner, Clair M. "Natural killer cells." Current Biology 9, no. 19 (October 1999): R716. http://dx.doi.org/10.1016/s0960-9822(99)80464-3.

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Lanier, Lewis L., and Joseph H. Phillips. "Natural killer cells." Current Biology 2, no. 3 (March 1992): 134. http://dx.doi.org/10.1016/0960-9822(92)90254-8.

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Dissertations / Theses on the topic "Killer cells"

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El-Sherbiny, Yasser Mohamed. "Natural killer cells and plasma cell neoplasia." Thesis, University of Leeds, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.438481.

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Chisholm, S. E. "Natural killer cell recognition of virally infected cells." Thesis, University of Cambridge, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597615.

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Natural killer (NK) cells are known to be important for the control of viral infections, particularly infection with large double stranded (ds)DNA viruses such as herpes simplex virus type 1 (HSV-1) and vaccinia virus (VV), but the pathways and interactions important for NK cell recognition of virally infected cells are not well understood. Thus, the aim of this thesis was to study the molecular mechanisms of NK cell recognition of target cells infected with either HSV-1 or VV. Experiments using a set of HSV-1 mutants, deficient in one or more of the immediate early (IE) genes, demonstrated that expression of ICP0 alone was found to be sufficient to render HSV-1 infected target cells susceptible to NK attack, and killing assays demonstrated that the natural cytotoxicity receptors (NCRs) were involved in the NK mediated killing of HSV-1 infected targets. For VV, it was not possible to narrow down exactly which VV gene was sufficient for generating NK cell mediated susceptibility, but the data indicated that the VV gene or genes involved are expressed early, conserved within the poxvirus family, and as such, likely to be essential for the virus. Flow cytometry experiments demonstrated that altered susceptibility of the target cells to NK cell lysis was due to upregulation of ligands for the NCRs, and the importance of the NCRs in NK mediated killing of VV infected targets was confirmed by killing assays. In addition, flow cytometry experiments demonstrated very little down regulation of MHC class I followed infection by either HSV-1 or VV, implying that MHC class I down regulation is not of major importance in NK mediated killing of infected cells.
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Nassiry, Ladan 1962. "Kinetics of Natural Killer (NK) cells in mice having elevated Natural Killer cell activity." Thesis, McGill University, 1986. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=65512.

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Damico, Nicole. "Preparing and Cloning a Natural Killer Cell Hybridoma." Youngstown State University / OhioLINK, 2000. http://rave.ohiolink.edu/etdc/view?acc_num=ysu1004458025.

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Mahmood, Sajid. "Diverse regulation of natural killer cell functions by dendritic cells." Public Library of Science, 2012. http://hdl.handle.net/1993/23963.

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Natural killer (NK) cells are innate lymphocytes with inherent ability to eliminate infected cells and produce several cytokines/chemokines. They express surface receptors to sense environment and interact with other immune cells including the Dendritic cells (DC). Reciprocally, DCs are also shown to activate NK-cells. NK/DC cross-talk is well-documented, yet the molecular interactions and the diverse NK-cell activities regulated by DC remain unclear. Several target proteins such as MHC-1, Qa-1 mediate NK-cell target recognition. One such antigen, Ocil/Clr-b functions as a cognate ligand of NKR-P1B/D, NK-inhibitory receptor. In first aim of my study, I documented that deficiency of Ocil/Clr-b expression not only augmented the sensitivity of DC towards NK-cell cytotoxicity but also regulated the development of mature NK-cells. Thus suggesting NKR-P1B/D:Ocil to be another receptor:ligand system, besides Ly49:MHC-1, that regulates NK-cell responsiveness. Src homology region 2-containing protein tyrosine phosphatase-1 (SHP-1) transmits inhibitory signals of the specific NK-inhibitory receptors, including NKRP-1B/D. SHP-1 silenced NK-cells showed unaffected target recognition towards prototypic target cells in this study. In addition, these cells also displayed an unexpected phenotype of self-killing in-vitro, thus implicated SHP-1 as an important regulator of some other unappreciated NK-cell functions. The data from my third study suggest that DCs are directly implicated in the induction of NK-cell migration. In summary, using a novel live-cell imaging microfluidic platform and conventional transwell migration assay this project established a clear molecular link between DC-derived soluble factors such as IP-10 and NK cell-chemokine receptor such as CXCR3. Previously, GM-CSF was shown as an inflammatory cytokine, involved in the development of DC as well as in mediating Th-1 immune responses. In this study I found that GM-CSF regulates NK-cell migration negatively. Lastly, the fourth aim of my thesis highlighted the critical role of immature-DC in the induction of maturation receptors (NK1.1 & Ly49) on differentiating NK-cells. I successfully established a multi-stage in-vitro NK-cell differentiation model and found that differentiating NK-cells required an active engagement with DCs, in addition to the soluble factors. I believe my PhD project findings would impact the existing knowledge to harness DC-based NK cell therapies in clinical settings.
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Evans, James Henry. "The interactions of human Natural Killer cells with accessory cells." Thesis, Imperial College London, 2011. http://hdl.handle.net/10044/1/6374.

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Natural Killer (NK) cells are lymphocytes of the innate immune system. However, there is increasing evidence that they can also play important roles in the adaptive immune system; as initiators, through antigen presentation; as effectors, via early release of IFN-y; and as immunoregulators, by eliminating over-activated macrophages. The functions of NK cells in these roles are intimately linked to their interactions with other cells during an immune response, for example recognition of target cells via activating receptors. The activating receptor NKG2D recognises proteins that are not normally expressed at the surface of most cells but are up-regulated during a cellular ‘stress’ response. However, NKG2D ligands can also be induced on human macrophages by TLR stimulation, leading to NK cell-mediated lysis. Here, I clarify that ligation of TLR4 preferentially up-regulates MICA but not MICB, TLR7/8 ligation up-regulated both MICA and MICB, while ligating TLR3, signalling through a MyD88-independent pathway, up-regulated neither. TLR4 stimulation decreased expression of microRNAs, miR-17-5, miR- 20a and miR-93, which target MICA, implicating a novel role for microRNAs in post-transcriptional regulation of NKG2D ligand expression. Moreover, the pathway involved IL-12/TNF- a-mediated autocrine signalling, thus incorporating an intrinsic mechanism for NK cell-mediated elimination of particularly activated macrophages. In addition to this immunoregulatory role, NK cell activity can shape a subsequent adaptive immune response. Subsets of NK cells can have distinct functions. Here, I demonstrate that following culture with IL-2, >25% of human peripheral blood NK cells express HLA-DR, due to an expansion of a small subset of NK cells expressing HLA-DR, in contrast to previous assumptions that HLADR is upregulated on previously negative cells. HLA-DR-expressing NK cells exhibited enhanced degranulation to susceptible target cells and expression of the chemokine receptor CXCR3, which facilitated their enrichment following exposure to CXCL11/I-TAC. Suggestive of an immunological role, stimulation of PBMCs with Mycobacterium bovis BCG triggered dramatic expansion of HLADR- expressing NK cells. In addition, the magnitude of the NK cell IFN-y secretion response in PBMC triggered by BCG was associated with the proportion of HLA-DR-expressing NK cells ex vivo. A direct contribution to the immune response was determined by specifically enriching the HLA-DR-expressing NK cell compartment, which substantially augmented the total NK cell IFN-y secretion response to BCG. Thus, HLA-DR expression marks a distinct subset of NK cells, present at low frequency in peripheral blood but readily expanded by IL-2, that can play a significant role during immune responses.
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El-Jawhari, Jehan Jomaa El-Said. "Tumour-mediated inhibition of natural killer cells." Thesis, University of Leeds, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.590426.

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The critical role of immune cells, in particular NK cells and cytotoxic T lymphocytes in recognition and elimination of tumour cells has been clearly demonstrated. However, immune evasion is a central hallmark of cancer; it negatively influences the prognosis and efficiency of therapies. Thus, understanding of this process will help to improve cancer therapy. Genetic alterations such as activation of oncogenes and loss of tumour suppressor genes are highly implicated in carcinogenesis. This study shows that the presence of KRAS oncogene reduced the surface expression of MHC class I on colorectal tumour cells and lead to suppression of CTL response. In contrast, the expression of KRAS oncogene did not affect the susceptibility of colorectal tumour cells to NK. cell killing nor inhibit NK cell functions. This suggests that targeting of the KRAS oncogene in colorectal tumours to improve CTL responses would be of a therapeutic benefit. In contrast, loss of a tumour suppressor gene, VHL in renal tumour cells was associated with reduced inhibitory effects on NK cells. Further investigations into how tumour cells inhibit NK cells were performed via an assessment of the role for an immunosuppressive cytokine, TGF-β Interestingly, the data show that TGF-β participates in colorectal tumour-mediated modification of the surface expression of NK cell receptors as well as suppression of NK cell functions. Supporting in vitro results, malignant ovarian tumour cells (ascitic-derived) had an inhibitory effect on the phenotype and activities of NK cells. Importantly, TGF-β was involved in these suppressive effects. My data strongly support targeting of TGF-β in therapy of colorectal and ovarian cancers to enhance anti-tumour responses ofNK cells.
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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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Stringaris, Katherine. "Natural killer cells and acute myeloid leukaemia." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/18014.

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Despite successful induction chemotherapy, most patients with acute myeloid leukemia (AML) will relapse. Immune surveillance by T cells or natural killer (NK) cells may play a role in preventing relapse. This thesis examines the potential of NK cells to control AML. Study 1 explored in 248 patients with haematological malignancies from the US National Institutes of Health, the genetic diversity of NK killer immunoglobulin receptor (KIR) genes in patients and their stem cell donors and their impact on outcome after stem cell transplantation (SCT) for haematological malignancy. Individuals with AML receiving SCT from donors inheriting 3 particular B-haplotype KIRs were 4 times less likely to relapse than those with donors without these favourable KIRs. Study 2 explored in samples obtained from 499 patients enrolled on UK MRC/NCRI AML trials, whether KIR genotype affects the risk of developing AML or the outcome of remission induction chemotherapy. While KIRs had no effect on the development or outcome of de novo AML, individuals with more activatory KIRs, in particular 2DS2, developed significantly less secondary AML, suggesting that activatory KIRs can protect against secondary AML. These studies support a role for NK-mediated immune surveillance in AML. Study 3 investigated the phenotype and function of AML NK cells. In 32 prospectively collected samples from AML patients undergoing remission induction chemotherapy at the Hammersmith Hospital, AML patients were found to have reduced NK activatory receptors, increased NK inhibitory receptors, and reduced cytotoxic function towards leukaemia, compared to healthy donors. These abnormalities corresponded with failure to achieve remission and can be induced in normal NK incubated with AML blasts. I conclude that KIR genetics have a limited influence on AML development and outcome but that AML itself can impair NK function, reducing the chance of achieving remission. These findings have implications for NK based immunotherapy for AML.
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Senff, Tina [Verfasser], and Jörg [Akademischer Betreuer] Timm. "The role of Natural Killer cells and Natural Killer T cells in HCV infection / Tina Senff ; Betreuer: Jörg Timm." Duisburg, 2018. http://d-nb.info/1153338009/34.

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Books on the topic "Killer cells"

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Palmer, Jon. Natural killer cells. Bethesda, MD: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Cancer Institute, International Cancer Research Data Bank, 1988.

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Vivier, Eric, James Di Santo, and Alessandro Moretta, eds. Natural Killer Cells. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-23916-3.

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Somanchi, Srinivas S., ed. Natural Killer Cells. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3684-7.

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Zimmer, Jacques, ed. Natural Killer Cells. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-02309-5.

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Brossay, Laurent. Everything you always wanted to know about NK cells but were afraid to ask. Trivandrum, Kerala, India: Transworld Research Network, 2007.

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Shimasaki, Noriko, ed. Natural Killer (NK) Cells. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2160-8.

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Terabe, Masaki, and Jay A. Berzofsky, eds. Natural Killer T cells. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-0613-6.

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Berke, Gideon. Killer lymphocytes. Dordrecht: Springer, 2004.

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1938-, Clark William R., ed. Killer lymphocytes. Dordrecht: Springer, 2005.

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Liu, Chaohong, ed. Invariant Natural Killer T-Cells. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1775-5.

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Book chapters on the topic "Killer cells"

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Ferlazzo, Guido. "Interactions Between NK Cells and Dendritic Cells." In Natural Killer Cells, 299–313. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-02309-5_16.

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Kokura, Satoshi. "Natural Killer Cells." In Immunotherapy of Cancer, 87–98. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55031-0_7.

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Wardle, E. Nigel. "Natural Killer Cells." In Guide to Signal Pathways in Immune Cells, 323–35. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-538-5_15.

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Rouzaire, Paul, Sébastien Viel, Jacques Bienvenu, and Thierry Walzer. "Natural Killer Cells." In Compendium of Inflammatory Diseases, 955–61. Basel: Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-7643-8550-7_142.

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Shepherd, David. "Natural Killer Cells." In Encyclopedia of Immunotoxicology, 654–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-54596-2_1058.

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Clausen, Torben, José Luis Trejo, Mark P. Mattson, Alexis M. Stranahan, Joanna Erion, Rosa Maria Bruno, Stefano Taddei, and Melinda M. Manore. "Natural Killer Cells." In Encyclopedia of Exercise Medicine in Health and Disease, 632. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2740.

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Rouzaire, Paul, Sébastien Viel, Jacques Bienvenu, and Thierry Walzer. "Natural Killer Cells." In Encyclopedia of Inflammatory Diseases, 1–8. Basel: Springer Basel, 2015. http://dx.doi.org/10.1007/978-3-0348-0620-6_142-4.

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Terme, Magali, Nathalie Chaput, and Laurence Zitvogel. "Interactions Between NK Cells and Regulatory T Cells." In Natural Killer Cells, 329–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-02309-5_18.

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Goetz, Deborah L. S., and William J. Murphy. "Natural Killer Cells and Their Role in Hematopoietic Stem Cell Transplantation." In Natural Killer Cells, 199–219. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-02309-5_10.

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Zingoni, Alessandra, Cristina Cerboni, Michele Ardolino, and Angela Santoni. "Modulation of T Cell-Mediated Immune Responses by Natural Killer Cells." In Natural Killer Cells, 315–27. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-02309-5_17.

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Conference papers on the topic "Killer cells"

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PIRAHMADIAN, ALIREZA, and SHAHRUDIN ABDUL. "Transgenic Natural Killer Cells." In Fifth International Conference On Advances in Applied Science and Environmental Engineering - ASEE 2016. Institute of Research Engineers and Doctors, 2016. http://dx.doi.org/10.15224/978-1-63248-086-6-54.

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Kennedy, Philippa (Pippa), Quinlan Kile, Blake Jacobson, Brianna Ettestad, Nicholas Zorko, Caroline Hallstrom, Behiye Kodal, et al. "1202 Tri-specific killer engagers target natural killer cells towards mesothelioma." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.1202.

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Mitchell, Michael J., Elizabeth C. Wayne, Kuldeepsinh Rana, Chris B. Schaffer, and Michael R. King. "Unnatural killer cells: TRAIL-coated leukocytes that kill cancer cells in the circulation." In 2014 40th Annual Northeast Bioengineering Conference (NEBEC). IEEE, 2014. http://dx.doi.org/10.1109/nebec.2014.6972880.

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Chan, Isaac S., Hildur Knútsdóttir, Gayathri Ramakrishnan, Veena Padmanaban, Manisha Warrier, Juan Carlos Ramirez, Matthew Dunworth, et al. "Abstract PO039: Cancer cells educate natural killer cells to a metastasis-promoting cell state." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 19-20, 2020. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/2326-6074.tumimm20-po039.

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Wiernik, Andres, and Jeffrey S. Miller. "Abstract 533: Dendritic cells are professional educators of Natural Killer cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-533.

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Mengistu, D. T., M. S. Toma, M. Busschots, K. Raslan, L. Mccloskey, J. L. Curtis, and C. M. Freeman. "Restoring Regulatory T Cells in COPD Could Dampen Natural Killer Cell Cytotoxicity." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a1243.

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Pecher, A. C., F. Kettemann, J. Henes, S. Duerr-Stoerzer, C. Schneidawind, L. Kanz, and D. Schneidawind. "FRI0408 Invariant natural killer t cells in systemic sclerosis." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.4531.

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Roth, Michèle, Selina Steiner, Christoph Bisig, Pierre Comte, Jan Czerwinski, Barbara Rothen-Rutishauser, Philipp Latzin, and Loretta Müller. "Effect of gasoline exhaust emission on bronchial epithelial cells and natural killer cells." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa4104.

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Yang, Lili, Drake Smith, Siyuan Liu, Sunjong Ji, and Bo Liu. "Abstract 3769: Stem cell-engineered invariant natural killer T cells for 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.am2017-3769.

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Lanier, Lewis L. "Abstract IA8: Natural killer cells in host defense against cancer." In Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-ia8.

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Reports on the topic "Killer cells"

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Chen, Xiuxu, and Jenny E. Gumperz. Human CD1d-Restricted Natural Killer T (NKT) Cell Cytotoxicity Against Myeloid Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2006. http://dx.doi.org/10.21236/ada462826.

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Paget, Christophe, Helene Duret, and Mark J. Smyth. Role of Natural Killer T Cells In Immunogenic Chemotherapy for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada571626.

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Paget, Christophe, Helene Duret, and Mark J. Smyth. Role of Natural Killer T Cells in Immunogenic Chemotherapy for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada595285.

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Senthil, Priyanka, and Hariharan Balakrishnan. The Engineering of Natural Killer Cells as an Emerging Adoptive Cancer Immunotherapy. Journal of Young Investigators, November 2020. http://dx.doi.org/10.22186/jyi.38.5.36-42.

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Pilones, Karsten A. Mechanisms of Invariant Natural Killer T Cell-Mediated Immunoregulation in Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2012. http://dx.doi.org/10.21236/ada589025.

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Bennett, Michael. Molecular Basis of Natural Killer Cell Tumor Target Recognition: The NKr/MHC Class I Complex. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada398189.

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Hasemann, Charles A. Molecular Basis of Natural Killer Cell Tumor Target Recognition: The NKr/MHC Class I Complex. Fort Belvoir, VA: Defense Technical Information Center, October 1999. http://dx.doi.org/10.21236/ada391281.

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Levy, Sandra M., Ronald B. Haberman, Theresa Whiteside, and Anne Simons. Stress, Coping, and Infectious Illness: Persistently Low Natural Killer Cell Activity as a Host Risk Factor. Fort Belvoir, VA: Defense Technical Information Center, October 1988. http://dx.doi.org/10.21236/ada202830.

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Levy, Sandra M., Ronald B. Herberman, Theresa Whiteside, and Anne Simons. Stress, Coping, and Infectious Illness: Persistently Low Natural Killer Cell Activity as a Host Risk Factor. Fort Belvoir, VA: Defense Technical Information Center, December 1990. http://dx.doi.org/10.21236/ada230422.

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Varbanova, Viktoria, Snejina Mihailova, Elissaveta Naumova, and Anastasiya Mihaylova. Distribution of Killer-cell Immunoglobulin-like Receptors (KIR) and their HLA Class I Ligands in the Bulgarian Population. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, July 2020. http://dx.doi.org/10.7546/crabs.2020.07.14.

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