Log in

Relevant bibliographies by topics / NK cell biology

Contents

Journal articles
Dissertations / Theses
Books
Book chapters

Academic literature on the topic 'NK cell biology'

Author: Grafiati

Published: 19 February 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'NK cell biology.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "NK cell biology"

1

Tarazona, Raquel, Nelson Lopez-Sejas, Beatriz Guerrero, Fakhri Hassouneh, Isabel Valhondo, Alejandra Pera, Beatriz Sanchez-Correa, et al. "Current progress in NK cell biology and NK cell-based cancer immunotherapy." Cancer Immunology, Immunotherapy 69, no. 5 (March 4, 2020): 879–99. http://dx.doi.org/10.1007/s00262-020-02532-9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Beaulieu, Aimee M., Natalie A. Bezman, Jang Eun Lee, Mehrdad Matloubian, Joseph C. Sun, and Lewis L. Lanier. "MicroRNA function in NK-cell biology." Immunological Reviews 253, no. 1 (April 2, 2013): 40–52. http://dx.doi.org/10.1111/imr.12045.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Thomas, Louis, and Eric Long. "NK cell licensing modulates NK cell conjugation to target cells via altered activation receptor function (P1063)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 121.3. http://dx.doi.org/10.4049/jimmunol.190.supp.121.3.

Full text

Abstract:

Abstract MHC class I recognition by inhibitory receptors on natural killer (NK) cells promotes a state of increased NK cell responsiveness through a process known as licensing/education. In the absence of either MHC class I expression or inhibitory receptors, NK cells exhibit a decreased responsive state. Thus NK cell licensing is a critical aspect of NK cell biology. However, understanding how licensing modulates natural cytotoxicity is limited. Using pure populations of unlicensed human NK cells, we were able to evaluate the effect of licensing on several NK cell functions. Our findings reveal that NK cell licensing does not affect lytic granule polarization but significantly enhances NK cell conjugation to target cells. Furthermore, our data show that activation receptors in unlicensed NK cells fail to provide strong ‘inside-out’ signaling for the beta2 integrin LFA-1. NK cell adhesion to target cells is a crucial initial step in NK cell-mediated cytotoxicity. The reduced conjugation of unlicensed NK cells may contribute to their hyporesponsive state.

APA, Harvard, Vancouver, ISO, and other styles

4

Stanietsky, Noa, and Ofer Mandelboim. "Paired NK cell receptors controlling NK cytotoxicity." FEBS Letters 584, no. 24 (September 7, 2010): 4895–900. http://dx.doi.org/10.1016/j.febslet.2010.08.047.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Schönberg, Kathrin, Janna Rudolph, Isabelle Cornez, Peter Brossart, and Dominik Wolf. "The JAK1/JAK2 Inhibitor Ruxolitinib Substantially Affects NK Cell Biology." Blood 122, no. 21 (November 15, 2013): 16. http://dx.doi.org/10.1182/blood.v122.21.16.16.

Full text

Abstract:

Abstract Introduction We recently demonstrated that ruxolitinib (INCB018424), the first approved JAK1/JAK2 inhibitor for treatment of myelofibrosis (MF), exerts potent anti-inflammatory activity. This may at least in part explain higher infection rates observed in ruxolitinib-treated patients. NK cells are critical for cancer-immune surveillance and cytokine-mediated signals are central for proper NK cell activation. We here aimed to characterize in detail the effects of JAK1/2 inhibition on human NK cells. Methods Highly purified CD56+ NK cells were isolated from human peripheral buffy coats by magnetic bead isolation and subsequently exposed to increasing concentrations of ruxolitinib (0.1-10 µM). Cytokine (1000U/ml IL-2, 25ng/ml IL-15)-induced NK cell proliferation was analyzed by CFSE dilution. Phenotypic and functional NK cell activation markers (NKp46, NKG2D, Granzyme B, CD16, and CD69) were analyzed by flow cytometry (including CD107a expression for degranulation). NK cell function was tested by flow-cytometry-based killing assays and quantification of IFN-γ production upon stimulation with either MHC class I-deficient K562 target cells or cytokines (IL-12, IL-18). In addition, phenotypic and functional analyses were also tested during NK receptor activation via plate-bound activating NKp46 antibodies. Signaling events were analyzed by Western Blot analysis to detect phosphorylation of JAK1 and JAK2 as well as by applying phospho-flow technology to evaluate ruxolitinib-mediated changes of cytokine-dependent signalling cascades (pS6, pSTAT1, pSTAT3, pSTAT5, pERK, pAKT, pP38, and pZAP70). Results Our results demonstrate provide first evidence that ruxolitinib profoundly affects cytokine-induced NK cell activation. This includes a significant and dose-dependent reduction of NK cell proliferation, reduced induction of activation-associated surface markers (including NKp46, NKG2D, Granzyme B, CD16, CD69) as well as impaired killing activity against the classical NK target cell line K562. In addition, all main functional activities of NK cells are down-regulated as shown by reduced cytotoxic capacity, impaired degranulation and IFN-γ production. After wash-out, the inhibitory effects of ruxolitinib on NK cells are fully reversible, as shown by proper re-activation by cytokines. In contrast to cytokine-mediated NK cell activation, stimulation via the NK-specific receptor NKp46 are not affected by ruxolitinib. Of note, ruxolitinib does not affect NK cell viability. On a molecular level, phospho-flow analyses revealed that cytokine associated signaling events, such as phosphorylation of STAT5 and S6 were dose-dependently reduced by ruxolitinib in primary human NK cells. Conclusions Ruxolitinib strongly inhibits NK cell activation leading to impaired proliferation and functional activity. Experiments verifying these effects in patients are currently ongoing and will be presented at the meeting. Our findings may have important clinical implications, when considering the application of ruxolitinib as GvHD therapy, because NK cells are critically involved in the GvL effect after allogeneic stem cell transplantation. Disclosures: Wolf: Novartis: Honoraria, Research Funding.

APA, Harvard, Vancouver, ISO, and other styles

6

Gardiner, Clair M. "NK cell metabolism." Journal of Leukocyte Biology 105, no. 6 (January 24, 2019): 1235–42. http://dx.doi.org/10.1002/jlb.mr0718-260r.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Vojvodic, Svetlana, and Stevan Popovic. "Natural killer cells: Biology, functions and clinical relevance." Medical review 63, no. 1-2 (2010): 91–97. http://dx.doi.org/10.2298/mpns1002091v.

Full text

Abstract:

Introduction. Natural Killer cells (NK cells) represent the subset of peripheral lymphocytes that play critical role in the innate immune response to virus-infected and tumor transformed cells. Lysis of NK sensitive target cells could be mediated independently of antigen stimulation and without requirement of peptide presentation by the major histocompatibility complex (MHC) molecules. NK cell activity and functions are controlled by a considerable number of cell surface receptors, which exist in both inhibitory and activating isoforms. There are several groups of NK cell surface receptors: 1) killer immunoglobulin like receptors-KIR, 2) C-type lectin receptors,3)natural citotoxicity receptors-NCR and 4) Toll-like receptors-TLR. Functions of NK receptors. Defining the biology of NK cell surface receptors has contributed to the concept of the manner how NK cells selectively recognize and lyse tumor and virally infected cells while sparing normal cells. Further, identification of NK receptor ligands and their expression on the normal and transformed cells has led to the development of clinical approaches to manipulating receptor/ligand interactions that showed clinical benefit. NK cells are the first lymphocyte subset that reconstitute the peripheral blood following allogeneic HSCT and multiple roles for alloreactive donor NK cells have been demonstrated, in diminishing Graft vs. Host Disease (GvHD) through selective killing recipient dendritic cells, prevention of graft rejection by killing recipient T cells and participation in Graft vs. Leukaemia (GvL) effect through destruction of residual host tumor cells. Conclusion. Besides their role in HSCT, NK cell receptors have an important clinical relevance that reflects from the fact that they play a crucial role in the development of some diseases as well as in possibilities of managing all NK receptors through selective expansion and usage of NK cells in cancer immunotherapy.

APA, Harvard, Vancouver, ISO, and other styles

8

Terrén, Iñigo, Ane Orrantia, Idoia Mikelez-Alonso, Joana Vitallé, Olatz Zenarruzabeitia, and Francisco Borrego. "NK Cell-Based Immunotherapy in Renal Cell Carcinoma." Cancers 12, no. 2 (January 29, 2020): 316. http://dx.doi.org/10.3390/cancers12020316.

Full text

Abstract:

Natural killer (NK) cells are cytotoxic lymphocytes that are able to kill tumor cells without prior sensitization. It has been shown that NK cells play a pivotal role in a variety of cancers, highlighting their relevance in tumor immunosurveillance. NK cell infiltration has been reported in renal cell carcinoma (RCC), the most frequent kidney cancer in adults, and their presence has been associated with patients’ survival. However, the role of NK cells in this disease is not yet fully understood. In this review, we summarize the biology of NK cells and the mechanisms through which they are able to recognize and kill tumor cells. Furthermore, we discuss the role that NK cells play in renal cell carcinoma, and review current strategies that are being used to boost and exploit their cytotoxic capabilities.

APA, Harvard, Vancouver, ISO, and other styles

9

Clara, Joseph A., Robert Reger, Mala Chakraborty, Steven L. Highfill, Jianjian Jin, David F. Stroncek, and Richard W. Childs. "Cell Density of NK Cells during Ex Vivo Expansion Impacts NK Cell Surface TRAIL Expression." Blood 136, Supplement 1 (November 5, 2020): 5–6. http://dx.doi.org/10.1182/blood-2020-141487.

Full text

Abstract:

Introduction Natural Killer (NK) cells are an emerging form of cancer immunotherapy currently being tested in clinical trials world-wide. NK cells are innate immune cells that can kill tumor cells via release of cytotoxic granules and via surface expression of the death receptor ligands tumor-related apoptosis-inducing ligand (TRAIL) and Fas ligand. We and others have recently shown that the proteasome inhibitor bortezomib sensitizes tumor cells to NK cell TRAIL-mediated killing by upregulation of death receptor 5. In a recent phase I NK cell dose-escalation study conducted at the NIH (NCT00720785) we have attempted to exploit TRAIL sensitization by administering ex vivo-expanded autologous NK cells to patients with solid tumors or hematologic malignancies that have been pretreated with bortezomib. Ex vivo cultures used to expand clinical grade NK cells for this trial utilize irradiated EBV-LCL feeder cells and IL-2 containing media which upregulates surface expression of TRAIL, substantially augmenting NK cell killing of bortezomib-treated tumors in vitro. Here we characterize the impact of specific expansion conditions used to generate high numbers of NK cells for clinical use on NK cell TRAIL expression. Methods To generate clinical grade ex vivo-expanded NK cells, we first isolated NK cells from patient apheresis products by CD3+ depletion followed by CD56+ selection, and stimulated these enriched NK cells with irradiated EBV-LCL feeder cells at a ratio of 1:10 in X-VIVO 20 supplemented with 10% inactivated human AB serum and recombinant human IL-2 (500 IU/ml). The clinical trial evaluated 8 escalating NK cell dose levels (Figure 1). Cohorts 1-4 received a single infusion of ex vivo-expanded NK cells on day 0 in a dose-escalating fashion (3-6 pts per cohort) and cohorts 5-7 received 1 x 108 NK cells/kg on day 0 and a second escalating dose of NK cells infused on day +5. A "closed bag" Baxter PL732 culture system was used for cohorts 1-7 which was later changed to a GREX500-CS (Wilson Wolf) system in cohorts 7-8. Using flow cytometry, we monitored surface expression of TRAIL on the day NK cells were harvested and infused fresh into patients. We also assessed TRAIL expression on NK cells from a single patient cultured at 6 different cell densities (range: 2.03-16.95 x 106/cm2) using culture conditions mimicking the phase I trial. Results A total of 137 NK cell cultures were harvested and administered fresh to 32 patients. NK cells on the day of harvest expanded a median of 198-fold, 895-fold, and 3637-fold on culture days 14-16, 19-22, and 24-27, respectively. NK cells at harvest contained a median of 99.7% CD3−/CD56+ NK cells, were 68.65% CD16+ and had a median of 88% viability. TRAIL was assessed by mean fluorescence intensity (MFI) with a median surface expression of of 1245 (range 132-4913) at the time of infusion (Figure 1). Expansions for cohort 8 generated 10-14 x109 (1 vessel) and 50-70 x109 NK cells (4-5 vessels) for fresh infusion, enough to support the target dose level of 1x108 (1st harvest) and 5x108 (2nd harvest) NK cells/kg. Remarkably, NK cells grown at higher cell density to reach the target cell numbers for cohort 8 exhibited substantially reduced TRAIL expression (median: 255, range 132-691). Subsequent experiments conducted on NK cells expanded in vitro for 14 days at different cell densities/concentrations showed TRAIL expression (MFI range: 319-1627) inversely correlated with both cell density and concentration (Figure 2). NK cells grown at the highest cell density (16.95 x 106/cm2) and concentration (4.23 x 106/mL) expressed the least amount of TRAIL (MFI 319), in contrast to those cultured at the lowest cell density (2.03 x 106/cm2) and concentration (0.51 x 106/mL), which demonstrated a TRAIL MFI of 1627. Conclusions Although ex vivo cultures using feeder cells make it possible to expand large numbers of NK cells for clinical use in humans, the higher concentrations and density of cells in these cultures reduce NK cell surface expression of TRAIL. In vitro, TRAIL expression appears to inversely correlate with cell density. These data highlight the need to avoid overly concentrating ex vivo expanded NK cells to maximize TRAIL surface expression as a method to potentiate the anticancer effects of adoptively infused NK cells. Disclosures No relevant conflicts of interest to declare.

APA, Harvard, Vancouver, ISO, and other styles

10

Lee, Barclay J., and Emily M. Mace. "Acquisition of cell migration defines NK cell differentiation from hematopoietic stem cell precursors." Molecular Biology of the Cell 28, no. 25 (December 2017): 3573–81. http://dx.doi.org/10.1091/mbc.e17-08-0508.

Full text

Abstract:

Human natural killer (NK) cells are generated from CD34+ precursors and can be differentiated in vitro by coculture with developmentally supportive stromal cells. We have previously described the acquisition of cell migration as a feature of NK cell terminal maturation in this system. Here we perform continuous long-term imaging and tracking of NK cell progenitors undergoing in vitro differentiation. We demonstrate that NK cell precursors can be tracked over long time periods on the order of weeks by utilizing phase-contrast microscopy and show that these cells acquire increasing motility as they mature. Additionally, we observe that NK cells display a more heterogeneous range of migratory behaviors at later stages of development, with the acquisition of complex modes of migration that are associated with terminal maturation. Together these data demonstrate previously unknown migratory behaviors of innate lymphocytes undergoing lineage differentiation revealed by long-term imaging and analysis workflows.

APA, Harvard, Vancouver, ISO, and other styles

More sources

Dissertations / Theses on the topic "NK cell biology"

1

Agüera-González, Sonia. "Cell biology on NKG2D ligands and NK cell recognition." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609348.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Trundley, Anita Elizabeth. "Aspects of human uterine NK cell biology." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.620028.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Mohan, Bindu. "Role of Siglec-7 in ganglioside recognition and modulating NK cell biology." Thesis, University of Dundee, 2013. https://discovery.dundee.ac.uk/en/studentTheses/93d42a43-7c3c-4d6e-b69a-27cb4673c1db.

Full text

Abstract:

Sialic acid binding Ig-like lectin-7 (Siglec-7), expressed primarily on NK cells, binds preferentially to alpha2,8 linked disialic acids such as present in the ganglioside GD3 that is upregulated in certain cancers. Siglec-7 is classified as an inhibitory receptor as it contains immunoreceptor tyrosine based inhibitory motifs. It has been shown to inhibit NK cytotoxicity in cellular assays thereby implying a role for it in NK cell mediated tumour surveillance. The aim of this project was to study factors affecting ligand recognition by Siglec-7 and its impact on NK cell functions. An investigation into the mechanism by which Siglec-7 mediates inhibitory signals to regulate NK cell biology was also carried out. Recognition of Siglec-7 for GD3 has been reported to be altered in the presence of complex gangliosides. This project was initiated with an aim to examine the role of such cis-interactions between GD3 and other gangliosides such as GM1 in biological systems and thereby its impact on NK cell biology. B16 (78) cell line was genetically modified to over-express both GD3 and GM1. This model system was then analysed using Siglec-7-Fc precomplexes for the recognition of GD3. Siglec-7-Fc binding of B16 (78) cells with high expression of GD3 and GM1 was significantly lower compared to cells having high expression of GD3 and low expression of GM1. However further investigation of these cis-interactions by confocal microscopy revealed that only less than 3% of the cells had patches of co-localization of the two gangliosides. Such lateral segregation of co-expressed GD3 and GM1 was also observed in another cell line model. Next, an investigation into the role of GD3 in modulating NK cell functions via Siglec-7 was carried out. Primary PBMCs and a Siglec-7 deficient NK cell line, NK92, were used for this purpose. The data obtained showed that Siglec-7 could negatively modulate NK cytotoxicity towards targets expressing disialylated ligands such as GD3. Furthermore Siglec-7 was also able to modulate integrin functions on NK cells. LFA-1 mediated adhesion of effectors to ICAM-1-Fc coated plates and the polarization of perforin granules to ICAM-1- Fc coated beads were negatively affected by the expression of Siglec-7 in the NK92 cell line. Biochemical analysis of LFA-1 mediated signalling in NK92 cells showed negative regulation of Src kinase activation, in an Siglec-7 dependent manner. Overall these findings suggest a role for Siglec-7 in modulating NK cell recognition of tumours with aberrant glycosylation patterns. They also form the basis of further investigation into the mechanisms of inhibitory signalling mediated by Siglec-7 and could therefore be of potential clinical relevance in NK cell mediated tumour clearance.

APA, Harvard, Vancouver, ISO, and other styles

5

El-Maghraby, Nermine Mostafa. "Modulation of BLT1 expression in human NK cells by selected cytokines." Mémoire, (Accès réservé UdeS) Droit de reproduction illimitée uniquement pour la création de matériel didactique, 2007. http://savoirs.usherbrooke.ca/handle/11143/3894.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Meredith, Tobias. "The regulatory effects of CD161 and MAIT cells." Thesis, Federation University Australia, 2020. http://researchonline.federation.edu.au/vital/access/HandleResolver/1959.17/176644.

Full text

Abstract:

Mucosal associated invariant T (MAIT) cells are connected with the potential regulation of anti-tumour responses, although their role in this regulation is poorly defined. In cancer, the relative frequency of MAIT cells has an impact on patient outcome, although how this impact is mediated is not known. Therefore, we have carefully modulated the frequency of MAIT cells within cultures and assessed the effect this has on the anti-tumour functions of important immune cells such as NK and conventional T cells. We identified that changes in MAIT cell frequency can significantly impact the ability of NK cells to become activated and produce proinflammatory cytokines. Interestingly, changes in MAIT cell frequency do not impact conventional T cell activation, but can alter pro-inflammatory cytokine expression. We also identified trends that suggest alterations in MAIT cell frequency may suppress a broad range of cytokines produced within the PBMC pool. The thesis also examined the potential regulatory impact of the cell surface molecule CD161 on T cells (particularly MAIT cells). Several distinctive characteristics have been identified that provides a broader understanding of the effect ligating and blocking this molecule can have. We have demonstrated that interaction with CD161 can promote activation and affect cytokine and perforin expression by MAIT cells. Conventional T cells are also affected, specifically their cytokine expression and activation. Lastly, we also performed several pilot studies, which identified changes in the expression of some genes of interest (e.g. IL-13, IL-5) and raised the possibility that the products of these genes could also be affected. Taken together, our research indicates that MAIT cell frequency can have significant effects on the anti-tumour roles of other immune cells. Additionally, we have furthered the understanding of which anti-tumour functions CD161 interaction can affect. CD161 has the potential to be used as an immunotherapeutic target in cancer patients, but more knowledge is required to determine the host of potential functions CD161 may affect. We suggest that further study is required, particularly in determining the effect CD161 ligation and blocking can have on cytokine output on a range of cells, including MAIT cells.
Doctor of Philosophy

APA, Harvard, Vancouver, ISO, and other styles

7

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Pyzik, Michal. "Immunogenetics of infection: MHC class I molecules and NK cell receptors interplay in the recognition of MCMV-infected cell and infection outcome." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116853.

Full text

Abstract:

Human cytomegalovirus (HCMV) is a herpesvirus found commonly in the world population, causing a severe and potentially fatal disease in neonates and immunocompromised patients. Clinical and experimental data indicate that a subset of innate lymphocytes, natural killer (NK) cells, plays a crucial role in resistance to infection. As infection with mouse CMV (MCMV) shares many pathophysiological aspects with the human disease, the mouse represents an excellent model to study CMV infection. The outcome of MCMV infection depends on the host genetic background and thus varies among the multiple inbred mouse strains. Importantly, mouse NK cells, through the expression of germ line encoded receptors, have the ability to recognize CMV infection, resulting in NK cell activation and the destruction of the infected cells. In each strain NK cells express amongst others, different sets of activating and inhibitory Ly49 receptors, in the presence of strain-specific MHC class I molecules, some of which are natural ligands to Ly49 receptors. Nevertheless, the exact mode of NK cell recognition of infected cell and the impact on the outcome of infection are complex and not fully understood. In order to characterize the molecular mechanisms underlying innate resistance to MCMV, we have initiated a systematic study to identify the possible ligands of Ly49 receptors and the nature of their interaction. We assessed the ability of distinct activating and inhibitory Ly49 receptors to recognize MCMV infection, in the context of diverse MHC class I haplotypes in vitro and in vivo. We show that the cognate interaction between several activating Ly49 receptors and MHC class I molecules depends on the presence of the viral regulator of antigen presentation, gp34/m04. Furthermore, we illustrate that, analogous to activating Ly49 receptors, inhibitory Ly49 receptors can be triggered by MCMV infection. This complex interaction, conditional on the type of MHC class I molecules, results in a spectrum of innate immune control of MCMV spread. Altogether, our results identify the fundamental mechanisms of NK cell receptor function in the recognition and eradication of viral infection. These will provide new grounds to understand and manipulate human NK cells in response to viral infections.
Le cytomégalovirus humain (HCMV) est un herpèsvirus omniprésent dans la population mondiale, qui provoque des symptômes graves et potentiellement mortels chez les nouveau-nés et les patients immunodéprimés. Les données cliniques et expérimentales indiquent qu'un sous-ensemble de lymphocytes innés, dites tueuses naturelles (NK), joue un rôle crucial dans la résistance à l'infection. Comme l'infection par le CMV murin (MCMV) partage de nombreux aspects physiopathologiques de la maladie humaine, la souris constitue un excellent modèle pour étudier l'infection par le CMV. La susceptibilité au MCMV varie grandement selon les lignées de souris congéniques et ce, en fonction de leur patrimoine génétique. Plus précisément, chaque lignée de souris exprime une variété de récepteurs activateurs ou inhibiteurs spécifiques aux cellules NK, les récepteurs Ly49, parallèlement à des répertoires de CMH de classe I variés, dont certains sont des ligands naturels des récepteurs Ly49. En effet, les cellules NK, grâce à l'expression de ces récepteurs encodés dans la lignée germinale, ont la capacité de reconnaître une infection au CMV, ce qui entraîne leur activation et la destruction des cellules infectées. Néanmoins, le mode exact de reconnaissance des cellules infectées par les cellules NK et l'impact sur l'issue de l'infection sont complexes et encore mal compris. Afin de caractériser les mécanismes moléculaires qui sous-tendent la résistance innée au MCMV, nous avons entrepris une étude systématique des ligands possibles des récepteurs Ly49 et de la nature de leur interaction. Nous avons évalué la capacité de reconnaître l'infection MCMV de différents récepteurs Ly49 activateurs ou inhibiteurs, dans le contexte de divers haplotypes de CMH de classe I in vitro et in vivo. Nous démontrons que l'interaction spécifique entre plusieurs récepteurs Ly49 activateurs et des molécules du CMH de classe I dépend de la présence de gp34/m04, un régulateur viral de la présentation d'antigène. De plus, nous montrons que, comme les récepteurs Ly49 activateurs, les récepteurs Ly49 inhibiteurs peuvent aussi être stimulés par une infection au MCMV. Cette interaction complexe, qui dépend du type de molécules de CMH de classe I, se traduit par des niveaux variable de contrôle de la propagation du MCMV par le système immunitaire. Nos résultats mettent en évidence des mécanismes fondamentaux de la fonction des récepteurs des cellules NK dans la reconnaissance et l'éradication de l'infection virale, et fournissent de nouvelles avenues pour comprendre et manipuler la réponse des cellules NK humaines aux infections virales.

APA, Harvard, Vancouver, ISO, and other styles

9

Valentin-Torres, Alice M. "Bidirectional Natural Killer Cell and Dendritic Cell Interactions in HIV-1 Pathogenesis." Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1346268879.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Blaser, Bradley W. "Interleukin 15 and transplantation biology the interface of innate and adaptive immunity /." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1145978587.

Full text

APA, Harvard, Vancouver, ISO, and other styles

More sources

Books on the topic "NK cell biology"

1

Williams, Colton. NK Cell Receptors: Advances in Cell Biology and Immunology. States Academic Press, 2021.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

2

Querfeld, Christiane, Steven T. Rosen, and Jasmine Zain. T Cell and Nk Cell Lymphomas: From Biology to Novel Therapies. Springer International Publishing AG, 2019.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "NK cell biology"

1

Lucas, Mathias, Cedric Vonarbourg, Peter Aichele, and Andreas Diefenbach. "Studying NK Cell/Dendritic Cell Interactions." In Methods in Molecular Biology, 97–126. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-362-6_8.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Domaica, Carolina I., Jessica M. Sierra, Norberto W. Zwirner, and Mercedes B. Fuertes. "Immunomodulation of NK Cell Activity." In Methods in Molecular Biology, 125–36. New York, NY: Springer US, 2019. http://dx.doi.org/10.1007/978-1-0716-0203-4_9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Li, Qing. "NK Cell Assays in Immunotoxicity Testing." In Methods in Molecular Biology, 207–19. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-401-2_15.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Lanier, Lewis L. "Activating and Inhibitory NK Cell Receptors." In Advances in Experimental Medicine and Biology, 13–18. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5355-7_2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Kimura, Hiroshi. "EBV in T-/NK-Cell Tumorigenesis." In Advances in Experimental Medicine and Biology, 459–75. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-7230-7_21.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Sanborn, Keri B., Gregory D. Rak, Ashley N. Mentlik, Pinaki P. Banerjee, and Jordan S. Orange. "Analysis of the NK Cell Immunological Synapse." In Methods in Molecular Biology, 127–48. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-362-6_9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Ziqing, Chen, Andreas Lundqvist, and Kristina Witt. "Strategies and Techniques for NK Cell Phenotyping." In Methods in Molecular Biology, 105–14. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9650-6_6.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Floerchinger, Alessia, and Christine E. Engeland. "NK Cell Effector Functions and Bystander Tumor Cell Killing in Immunovirotherapy." In Methods in Molecular Biology, 233–48. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2441-8_12.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Li, Qing. "Natural Killer (NK) Cell Assays in Immunotoxicity Testing." In Methods in Molecular Biology, 231–41. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8549-4_15.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!