Relevant bibliographies by topics / Clec9A

Academic literature on the topic 'Clec9A'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Clec9A.'

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 "Clec9A"

1

Caminschi, Irina, Anna I. Proietto, Fatma Ahmet, Susie Kitsoulis, Joo Shin Teh, Jennifer C. Y. Lo, Alexandra Rizzitelli, et al. "The dendritic cell subtype-restricted C-type lectin Clec9A is a target for vaccine enhancement." Blood 112, no. 8 (October 15, 2008): 3264–73. http://dx.doi.org/10.1182/blood-2008-05-155176.

Full text
Abstract:
Abstract A novel dendritic cell (DC)–restricted molecule, Clec9A, was identified by gene expression profiling of mouse DC subtypes. Based on sequence similarity, a human ortholog was identified. Clec9A encodes a type II membrane protein with a single extracellular C-type lectin domain. Both the mouse Clec9A and human CLEC9A were cloned and expressed, and monoclonal antibodies (mAbs) against each were generated. Surface staining revealed that Clec9A was selective for mouse DCs and was restricted to the CD8+ conventional DC and plasmacytoid DC subtypes. A subset of human blood DCs also expressed CLEC9A. A single injection of mice with a mAb against Clec9A, which targets antigens (Ags) to the DCs, produced a striking enhancement of antibody responses in the absence of added adjuvants or danger signals, even in mice lacking Toll-like receptor signaling pathways. Such targeting also enhanced CD4 and CD8 T-cell responses. Thus, Clec9A serves as a new marker to distinguish subtypes of both mouse and human DCs. Furthermore, targeting Ags to DCs with antibodies to Clec9A is a promising strategy to enhance the efficiency of vaccines, even in the absence of adjuvants.
APA, Harvard, Vancouver, ISO, and other styles
2

Schreibelt, Gerty, Lieke J. J. Klinkenberg, Luis J. Cruz, Paul J. Tacken, Jurjen Tel, Martin Kreutz, Gosse J. Adema, Gordon D. Brown, Carl G. Figdor, and I. Jolanda M. de Vries. "The C-type lectin receptor CLEC9A mediates antigen uptake and (cross-)presentation by human blood BDCA3+ myeloid dendritic cells." Blood 119, no. 10 (March 8, 2012): 2284–92. http://dx.doi.org/10.1182/blood-2011-08-373944.

Full text
Abstract:
Abstract CLEC9A is a recently discovered C-type lectin receptor involved in sensing necrotic cells. In humans, this receptor is selectively expressed by BDCA3+ myeloid dendritic cells (mDCs), which have been proposed to be the main human cross-presenting mDCs and may represent the human homologue of murine CD8+ DCs. In mice, it was demonstrated that antigens delivered with antibodies to CLEC9A are presented by CD8+ DCs to both CD4+ and CD8+ T cells and induce antitumor immunity in a melanoma model. Here we assessed the ability of CLEC9A to mediate antigen presentation by human BDCA3+ mDCs, which represent < 0.05% of peripheral blood leukocytes. We demonstrate that CLEC9A is only expressed on immature BDCA3+ mDCs and that cell surface expression is lost after TLR-mediated maturation. CLEC9A triggering via antibody binding rapidly induces receptor internalization but does not affect TLR-induced cytokine production or expression of costimulatory molecules. More importantly, antigens delivered via CLEC9A antibodies to BDCA3+ mDCs are presented by both MHC class I (cross-presentation) and MHC class II to antigen-specific T cells. We conclude that CLEC9A is a promising target for in vivo antigen delivery in humans to increase the efficiency of vaccines against infectious or malignant diseases.
APA, Harvard, Vancouver, ISO, and other styles
3

Ito, Fumito, Mark D. Long, Ryutaro Kajihara, Satoko Matsueda, Takaaki Oba, Kazunori Kanehira, Song Liu, and Kenichi Makino. "Notch signaling is required for generation of conventional type 1 dendritic cells from human induced pluripotent stem cells." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 47.07. http://dx.doi.org/10.4049/jimmunol.208.supp.47.07.

Full text
Abstract:
Abstract Compelling evidence shows a critical role of conventional type 1 dendritic cells (cDC1) in T-cell mediated antitumor immunity; however, obtaining large numbers of cDC1 is difficult. Theoretically, this limitation can be overcome by using induced pluripotent stem cells (iPSC) that could provide an unlimited source of autologous cDC1. However, generation of cDC1 from human iPSC remains elusive. Here, we hypothesized that Notch signaling would facilitate generation of cDC1 from human iPSC. We found that human iPSC gave rise to CD141+XCR1+CLEC9A+HLA-DR+ cells on OP9 feeder cells expressing the Notch ligand delta-like 1 (OP9-DL1) while the majority of iPSC-derived cells differentiated on OP9 cells were monocytic cells. Single-cell RNA sequencing analyses confirmed the presence of cDC1 as well as identified the heterogeneity of iPSC-derived CD1c+ cells; cDC2A, cDC2B, CD5+cDC2, and DC3. Inhibition of Notch signaling during co-culture of iPSC-derived CD34+ hematopoietic progenitor cells with OP9-DL1 cells abrogated generation of cDC1, and made expression of CD5, CLEC4A, CLEC10A and CD163 in CD1c+ DC similar to those differentiated on OP9 cells. Notch-activated human iPSC-derived XCR1+CLEC9A+HLA-DR+CD11c+ cells exhibited similar gene expression profile with peripheral blood cDC1, and phagocytotic, T-cell proliferative, and cytokine producing functions. Our study demonstrates that Notch signaling is required for the differentiation of cDC1-like cells, and facilitates generation of various cDC subsets from human iPSC. These findings provide insights into the future development of personalized treatment with unlimited numbers of autologous cDC1 from human iPSC. This work was supported by National Cancer Institute (NCI) grant P30CA016056 involving the use of Roswell Park’s Flow and Image Cytometry, Bioinformatics, and Genomic Shared Resources. This work was supported by the Melanoma Research Alliance and the Sarcoma Foundation of America (F. Ito), Uehara Memorial Foundation (T. Oba), and National Cancer Institute (NCI) grant, U24CA232979 (M. Long and S. Liu), K08CA197966 and R01CA255240-01A1 (F. Ito).
APA, Harvard, Vancouver, ISO, and other styles
4

Masterman, Kelly-Anne, Oscar L. Haigh, Kirsteen M. Tullett, Ingrid M. Leal-Rojas, Carina Walpole, Frances E. Pearson, Jonathon Cebon, et al. "Human CLEC9A antibodies deliver NY-ESO-1 antigen to CD141+ dendritic cells to activate naïve and memory NY-ESO-1-specific CD8+ T cells." Journal for ImmunoTherapy of Cancer 8, no. 2 (July 2020): e000691. http://dx.doi.org/10.1136/jitc-2020-000691.

Full text
Abstract:
BackgroundDendritic cells (DCs) are crucial for the efficacy of cancer vaccines, but current vaccines do not harness the key cDC1 subtype required for effective CD8+ T-cell-mediated tumor immune responses. Vaccine immunogenicity could be enhanced by specific delivery of immunogenic tumor antigens to CD141+ DCs, the human cDC1 equivalent. CD141+ DCs exclusively express the C-type-lectin-like receptor CLEC9A, which is important for the regulation of CD8+ T cell responses. This study developed a new vaccine that harnesses a human anti-CLEC9A antibody to specifically deliver the immunogenic tumor antigen, NY-ESO-1 (New York esophageal squamous cell carcinoma 1), to human CD141+ DCs. The ability of the CLEC9A-NY-ESO-1 antibody to activate NY-ESO-1-specific naïve and memory CD8+ T cells was examined and compared with a vaccine comprised of a human DEC-205-NY-ESO-1 antibody that targets all human DCs.MethodsHuman anti-CLEC9A, anti-DEC-205 and isotype control IgG4 antibodies were genetically fused to NY-ESO-1 polypeptide. Cross-presentation to NY-ESO-1-epitope-specific CD8+ T cells and reactivity of T cell responses in patients with melanoma were assessed by interferon γ (IFNγ) production following incubation of CD141+ DCs and patient peripheral blood mononuclear cells with targeting antibodies. Humanized mice containing human DC subsets and a repertoire of naïve NY-ESO-1-specific CD8+ T cells were used to investigate naïve T cell priming. T cell effector function was measured by expression of IFNγ, MIP-1β, tumor necrosis factor and CD107a and by lysis of target tumor cells.ResultsCLEC9A-NY-ESO-1 antibodies (Abs) were effective at mediating delivery and cross-presentation of multiple NY-ESO-1 epitopes by CD141+ DCs for activation of NY-ESO-1-specific CD8+ T cells. When benchmarked to NY-ESO-1 conjugated to an untargeted control antibody or to anti-human DEC-205, CLEC9A-NY-ESO-1 was superior at ex vivo reactivation of NY-ESO-1-specific T cell responses in patients with melanoma. Moreover, CLEC9A-NY-ESO-1 induced priming of naïve NY-ESO-1-specific CD8+ T cells with polyclonal effector function and potent tumor killing capacity in vitro.ConclusionsThese data advocate human CLEC9A-NY-ESO-1 Ab as an attractive strategy for specific targeting of CD141+ DCs to enhance tumor immunogenicity in NY-ESO-1-expressing malignancies.
APA, Harvard, Vancouver, ISO, and other styles
5

Bell, Elaine. "CLEC9A: linking necrosis and immunity." Nature Reviews Immunology 9, no. 4 (April 2009): 223. http://dx.doi.org/10.1038/nri2531.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Masterman, Kelly-Anne, Oscar Haigh, Kirsteen Tullett, Ingrid Leal-Rojas, Carina Walpole, Frances Pearson, Jonathon Cebon, et al. "612 Human CLEC9A antibodies deliver NY-ESO-1 antigen to CD141+ dendritic cells to activate naïve and memory NY-ESO-1-specific CD8+ T cells." Journal for ImmunoTherapy of Cancer 8, Suppl 3 (November 2020): A648. http://dx.doi.org/10.1136/jitc-2020-sitc2020.0612.

Full text
Abstract:
BackgroundDendritic cells (DC) are crucial for the efficacy of cancer vaccines, but current vaccines do not harness the key cDC1 subtype required for effective CD8+ T cell mediated tumor immune responses. Vaccine immunogenicity could be enhanced by specific delivery of immunogenic tumor antigens to CD141+ DC, the human cDC1 equivalent. CD141+ DC exclusively express the C-type-lectin-like receptor CLEC9A, which is important for the regulation of CD8+ T cell responses. This study developed a new vaccine that harnesses a human anti-CLEC9A antibody to specifically deliver the immunogenic tumor antigen, NY-ESO-1 to human CD141+ DC. The ability of the CLEC9A-NY-ESO-1 antibody to activate NY-ESO-1 specific naïve and memory CD8+ T cells was examined and compared to a vaccine comprised of a human DEC-205-NY-ESO-1 antibody that targets all human DC.MethodsHuman anti-CLEC9A, anti-DEC-205 and isotype control IgG4 antibodies were genetically fused to NY-ESO-1 polypeptide. Cross-presentation to NY-ESO-1- epitope specific CD8+ T cells and reactivity of T cell responses in melanoma patients was assessed by IFNγ production following incubation of CD141+ DC and patient peripheral blood mononuclear cells with targeting antibodies. Humanized mice containing human DC subsets and a repertoire of naïve NY-ESO-1-specific CD8+ T cells were used to investigate naïve T cell priming. T cell effector function was measured by expression of IFNγ, MIP-1β, TNF and CD107a and by lysis of target tumor cells.ResultsCLEC9A-NY-ESO-1 Ab were effective at mediating delivery and cross-presentation of multiple NY-ESO-1 epitopes by CD141+ DC for activation of NY-ESO-1-specific CD8+ T cells. When benchmarked to NY-ESO-1 conjugated to an untargeted control antibody or to anti-human DEC-205, CLEC9A-NY-ESO-1 was superior at ex vivo reactivation of NY-ESO-1-specific T cell responses in melanoma patients. Moreover, CLEC9A-NY-ESO-1 induced priming of naïve NY-ESO-1-specific CD8+ T cells with polyclonal effector function and potent tumor killing capacity in vitro.ConclusionsThese data advocate human CLEC9A-NY-ESO-1 antibody as an attractive strategy for specific targeting of CD141+ DC to enhance tumour immunogenicity in NY-ESO-1-expressing malignancies.Ethics ApprovalWritten informed consent was obtained for human sample acquisition in line with standards established by the Declaration of Helsinki. Study approval was granted by the Mater Human Research Ethics Committee (HREC13/MHS/83 and HREC13/MHS/86) and The U.S. Army Medical Research and Materiel Command (USAMRMC) Office of Research Protections, Human Research Protection Office (HRPO; A-18738.1, A-18738.2, A-18738.3). All animal experiments were approved by the University of Queensland Animal Ethics Committee and conducted in accordance with the Australian Code for the Care and Use of Animals for Scientific Purposes in addition to the laws of the United States and regulations of the Department of Agriculture.
APA, Harvard, Vancouver, ISO, and other styles
7

Haddad, Y., L. Laurans, S. Metghalchi, Z. Zeboudj, A. Giraud, Z. Mallat, and S. Taleb. "The role of CLEC9a in atherosclerosis development." Archives of Cardiovascular Diseases Supplements 9, no. 2 (April 2017): 184. http://dx.doi.org/10.1016/s1878-6480(17)30455-x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

van der Aa, Evelyn, Nadine van Montfoort, and Andrea M. Woltman. "BDCA3+CLEC9A+ human dendritic cell function and development." Seminars in Cell & Developmental Biology 41 (May 2015): 39–48. http://dx.doi.org/10.1016/j.semcdb.2014.05.016.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Park, Hae-Young, Amanda Light, Mireille H. Lahoud, Irina Caminschi, David M. Tarlinton, and Ken Shortman. "Evolution of B Cell Responses to Clec9A-Targeted Antigen." Journal of Immunology 191, no. 10 (October 11, 2013): 4919–25. http://dx.doi.org/10.4049/jimmunol.1301947.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Shen, Lianjun, Janice BelleIsle, and Kenneth Rock. "Regulation of cross priming and anti-tumor immunity in vivo (107.2)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 107.2. http://dx.doi.org/10.4049/jimmunol.188.supp.107.2.

Full text
Abstract:
Abstract Cross priming plays an important role in immune surveillance against invading pathogens and cancers. The underlying mechanisms and regulation of this process, especially in vivo, are still not fully understood. The cross priming process in vivo is regulated and influenced by a number of factors at several levels. One factor is the state of the antigen donor cells. Another component is the contribution of innate immune receptors (TLR, CLR and NLR). We find that although the innate adaptor MyD88 is dispensable for cross priming of primary CD8 T cell responses, it is essential to generate long lasting anti-tumor immunity. Yet another factor that has been suggested is the participation of CD8α+Clec9a+ dendritic cells in cross presentation. However, we find that the primary CTL response primed by cell-associated antigen is largely unaffected or marginally compromised in mice lacking the CD8α+Clec9a+ DC subset, suggesting that other types of APCs also make a significant contribution. Taken together, many factors are involved in cross priming and its outcome.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Clec9A"

1

Haddad, Yacine. "Rôle de Clec9a dans l'athérosclérose." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCB099/document.

Full text
Abstract:
L’athérosclérose est une maladie inflammatoire chronique. L’une des caractéristiques des lésions d’athérosclérose est l’accumulation anormale de corps apoptotiques et nécrotiques, due à un défaut d’efferocytose, ceci entraînant la formation du cœur nécrotique. L’évolution de ce cœur nécrotique est également associée à une augmentation de l’inflammation et de la taille des plaques d’athérosclérose, mais aussi dans la survenue de complications telle que la rupture de plaque. Clec9a est un récepteur transmembranaire de type lectine C, majoritairement exprimé par une sous population de cellules dendritiques les DC-CD8α+. Il est capable de reconnaître un ligand spécifiquement exprimé par les corps nécrotiques, l’actine F. L’objectif de notre travail a été de savoir si Clec9a, qui est capable de reconnaître les corps nécrotiques, pouvait être impliqué dans la modulation de l’inflammation observée au cours du développement de l’athérosclérose. Au cours de cette étude, nous avons montré, in vivo partir de deux modèles murins (ApoE-/- et LDLr-/-), que la délétion de Clec9a entraîne une diminution significative de la taille des lésions dans un contexte d’hypercholestérolémie modérée. Cette athéro-protection observée en l’absence de Clec9a, est associée à une augmentation de l’expression de l’IL-10, qui est une interleukine anti-athérogène et anti-inflammatoire. Cet effet athéroprotecteur de l’absence de Clec9a n’est plus observé lorsque l’IL-10 est totalement invalidée. De plus, nous avons montré que l’invalidation de Clec9a spécifiquement dans les DC-CD8α+ entraîne, in vivo, une diminution de l’infiltration des macrophages et des lymphocytes T dans les lésions, ainsi qu’une augmentation de l’expression de l’IL-10, favorisant une diminution de la taille des lésions. La compréhension des mécanismes inflammatoires dans l’athérosclérose constitue un enjeu majeur pour prévenir les risques de complications comme la rupture de plaque ou la thrombose. Ainsi, ce travail met en évidence un nouveau rôle de Clec9a dans la régulation de l’inflammation dans l’athérosclérose et pourrait donc représenter une cible thérapeutique potentielle
Atherosclerosis is a chronic inflammatory disease. One of the characteristics of atherosclerotic lesions is the abnormal accumulation of apoptotic and necrotic cells, due to a deficiency of efferocytosis, which leads to the formation of the necrotic heart. The evolution of this necrotic core is also associated with an increase in inflammation and lesions of atherosclerosis, but also in the occurrence of complications such as plaque rupture. Clec9a is a C type lectin receptor, mainly expressed by a subpopulation of dendritic cells, which are the CD8α+ dendritic cells. This receptor is able to recognize a ligand expressed by necrotic cells, the actin F. The aim of our work was to find out if Clec9a, which can sense necrotic cells, could be involved in modulating the inflammation observed during the development of atherosclerosis. In this study, we have shown, in vivo with two mouse models (ApoE - / - and LDLr - / -), that the deletion of Clec9a leads to a significant decrease in the incidence of moderate hypercholesterolemia. This athero-protection observed in the absence of Clec9a, is associated with an increase in the expression of IL-10, which is an anti-atherogenic and anti-inflammatory cytokine. This athero-protective effect of the absence of Clec9a is abolished after total invalidation of IL-10. Furthermore, we report that specific knockdown of Clec9a in CD8α+-DC, in vivo, leads to a decrease in macrophage and lymphocyte infiltration in lesions, as well as an increase in IL-1 expression. 10, which promotes a decrease in lesions size. Understanding of inflammatory mechanisms in atherosclerosis is a major challenge to prevent the risk of complications such as plaque rupture or thrombosis. Thus, this work highlights a new role of Clec9a in the regulation of inflammation in atherosclerosis and could be therefore a potential therapeutic target
APA, Harvard, Vancouver, ISO, and other styles
2

Huysamen, Cristal. "The characterization of a novel C-type lectin-like receptor, CLEC9A." Doctoral thesis, University of Cape Town, 2008. http://hdl.handle.net/11427/3060.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Messerer, Denise [Verfasser], and Sven [Akademischer Betreuer] Reese. "Bedeutung Clec9a-abhängiger Immunzellen in kardialen Entzündungsprozessen / Denise Messerer ; Betreuer: Sven Reese." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2020. http://d-nb.info/1215499965/34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Van, Blijswijk J. M. "Mouse models to deplete or label dendritic cells via genetic manipulation of the Clec9a locus." Thesis, University College London (University of London), 2015. http://discovery.ucl.ac.uk/1472681/.

Full text
Abstract:
Dendritic cells (DCs) play important roles at the interface between innate and adaptive immunity by priming and directing T cell responses. Much of our current knowledge of DC biology has come from mouse models in which DCs can be genetically manipulated, labelled or ablated. Here, novel models are presented using a strategy that targets DC precursors via genetic editing of the Clec9a locus. While validating a novel mouse model to inducibly deplete DCs using diphtheria toxin receptor (DTR) expression driven by Clec9a, it became clear that these Clec9a+/CreROSAiDTR mice suffer from unexpected lymph node (LN) hypocellularity and reduced frequencies of DCs in LNs, even in the absence of diphtheria toxin (DT) injection. This phenotype turned out to be a common feature of other mouse models in which DTR is expressed on DCs (e.g. CD11c-DTR and Langerin-DTR mice) and raises questions about the interpretation of results obtained with such animals. Therefore, in an alternative approach, mice were developed to constitutively lack DCs by expressing the diphtheria toxin alpha (DTA) subunit under control of the Clec9a locus. Unfortunately, these mice still harboured DCs and only showed partial reduction of one DC subset. Finally, seeding of tissues by DC precursors was examined. Clec9a+/CreROSA+/confetti mice were generated in which DC precursors stochastically express one of four fluorescent proteins, which is inherited by its daughter cells. 8- Colour microscopy of tissue sections and histo-cytometry analysis of the images was developed to analyse these mice. This approach will be used to determine how many daughter cells are produced when a single DC precursor seeds the small intestine (clonal burst size), whether these daughters are found among different DC subsets and whether seeding changes during inflammation. In summary, manipulation of the Clec9a locus proves to be an excellent way to study the DC lineage and DC precursor behaviour in the mouse.
APA, Harvard, Vancouver, ISO, and other styles
5

Köhler, Arnaud. "Rôle des cellules dendritiques pre-CD8α Clec9A+ dans la protection contre Listeria monocytogenes en début de vie." Doctoral thesis, Universite Libre de Bruxelles, 2016. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/235619.

Full text
Abstract:
Selon un rapport de l’OMS, les maladies infectieuses figurent parmi les 3 causes les plus fréquentes de mortalité en début de vie. En effet, les nouveau-nés présentent une sensibilité particulièrement importante aux infections, de par leur système immunitaire toujours en développement et donc immature. Parmi les particularités de l’immunité néonatale, l’absence de cDCs CD11chigh CD8α+ durant la 1ère semaine de vie rend compte de l’incapacité du nouveau-né à développer des réponses de type Th1 et T CD8+ cytotoxiques, essentielles à la protection contre certains pathogènes comme Listeria monocytogenes (Lm). Mon travail de thèse a porté sur l’ontogénie des DCs conventionnelles CD11chigh CD8α+ et plus particulièrement sur la fonction de cette lignée de DCs en début de vie lors d’une infection par Lm. Au cours de cette étude, nous avons identifié, chez le nouveau-né, une population splénique de cDCs CD11chigh qui expriment les marqueurs CD24, CD205 et Clec9A mais pas le CD8α. Cette population, qui dépend du facteur de transcription Batf3, acquière le CD8α une fois transférée dans une souris adulte. Ces DCs néonatales, que nous nommerons DCs pre-CD8α Clec9A+, constituent donc les précurseurs des DCs CD8α+. L’étude fonctionnelle de ces DCs pre-CD8α Clec9A+ a montré qu’elles étaient capables de phagocyter Lm et de générer des réponses T CD8+ contre cette bactérie. De plus, ces cellules sécrètent de l’IL-12p40 et de manière unique de l’IL-10 en réponse à une stimulation par Lm. Par contre, contrairement aux cDCs CD8α+ adultes, nous n’avons observé aucune production d’IL-12p70 par les DCs pre-CD8α Clec9A+ en conditions physiologiques. Elles ne sécrètent pas non plus d’IL-23. Nous avons également montré que ces sécrétions d’IL-12p40 et d’IL-10 jouaient respectivement un rôle positif et négatif dans l’induction des réponses T CD8+ contre Lm. Ainsi, la génération des réponses T CD8+ contre Lm semble résulter, en début de vie, d’une balance entre la sécrétion de ces 2 cytokines aux propriétés antagonistes. Par ailleurs, nous avons démontré que ces cellules constituaient une cible privilégiée en vue d’améliorer les stratégies vaccinales en début de vie. En effet, l’administration à des nouveau-nés d’une construction anti-Clec9A/OVA, associée au poly(I:C), induit des réponses T CD8+ anti-Lm mémoires protectrices à l’âge adulte. Finalement, nous montrons que le TNF-α produit par les monocytes et les neutrophiles joue un rôle essentiel dans la génération des réponses T CD8+ en régulant notamment le statut et la fonction des DCs pre-CD8α Clec9A+ en début de vie. En effet, cette cytokine modifie, en faveur d’une production d’IL-12p40, la balance IL-12p40/IL-10 sécrétée par celles-ci. L’inhibition de la production d’IL-10 par le TNF-α pourrait s’expliquer au moins en partie par une inhibition de la β-caténine au sein des DCs pre-CD8α Clec9A+. En conclusion, nous avons caractérisé un précurseur des DCs CD8α+ biologiquement actif au sein de la rate du nouveau-né de 3 jours. Celui-ci représente une cible potentielle pour l’amélioration des stratégies vaccinales contre des bactéries intracellulaires ou des virus en début de vie, et ce pour autant que l’on puisse contrôler ses propriétés régulatrices.
Doctorat en Sciences biomédicales et pharmaceutiques (Médecine)
info:eu-repo/semantics/nonPublished
APA, Harvard, Vancouver, ISO, and other styles
6

Lodhia, Puja. "Investigating the intracellular interactions of CLEC14A and the characterisation of monoclonal antibodies targeting CLEC14A." Thesis, University of Birmingham, 2016. http://etheses.bham.ac.uk//id/eprint/7014/.

Full text
Abstract:
CLEC14A is a tumour endothelial marker known to regulate sprouting angiogenesis. While the extracellular interactions of CLEC14A have previously been studied, the intracellular interactions of CLEC14A are unknown. Fascin was identified as a binding partner for the cytoplasmic tail of CLEC14A using a yeast two hybrid screen. Interaction of CLEC14A with fascin was confirmed by proximity ligation and co-localisation was observed in HUVEC filopodia. This data indicated that interaction of CLEC14A and fascin may be important for filopodia formation during sprouting angiogenesis. Binding studies with domain deletion mutants of fascin revealed the CLEC14A binding site to be located within a highly conserved region of the β-trefoil 3 domain between amino acids 323 and 384. In addition, phosphorylation of S274 was found to regulate this interaction. Five monoclonal antibodies against CLEC14A had the potential to be developed into anti-angiogenic cancer therapeutics. The functional properties of these antibodies were explored in in vitro assays. Clones 1 and 3 were found to inhibit cell migration while clone 4 disrupted tubule formation. Clones 3 and 4 were developed into antibody drug conjugates (ADCs). These ADCs demonstrated potent cytotoxicity localised to the tumour endothelium in vivo. These results indicate that targeting CLEC14A could be an effective strategy to disrupt the tumour vasculature.
APA, Harvard, Vancouver, ISO, and other styles
7

Teng, Ooiean, and 丁瑋嫣. "Identification of CLEC5A in modulating host immune response after influenza A virus infection." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/208615.

Full text
Abstract:
Human infections with influenza A virus (IAV) exhibit mild to severe clinical outcomes as a result of differential virus-host interactions. C-type lectin receptors (CLRs) are pattern recognition receptors that may sense carbohydrates, proteins, or lipids derived from infected hosts or the invading microbes including bacteria, viruses, fungi, or parasites. CLR-viral interaction may lead to increased viral entry and spread; furthermore, their interactions have been reported to trigger downstream signaling that further modulates host’s innate immune responses through the induction of pro-inflammatory cytokines. To date, DC-SIGN and DC-SIGNR have been shown to mediate IAV entry; however, the potential interactions between other human transmembrane CLRs with IAV have not yet been systematically investigated. We utilized lentiviral-based pseudoparticles expressing influenza hemagglutinin (HA) to examine the binding potential between HA and a panel of human CLRs expressed in soluble form. CLEC5A was identified as a potential interacting target with the HA proteins derived from a highly pathogenic avian H5N1 virus A/VN/1203/04 (VN1203) or a human seasonal H1N1 virus A/HK/54/98 (HK5498), albeit at different binding intensity. Applying siRNA gene silencing, we confirmed that CLEC5A did not enhance influenza entry in human monocytic U937 cells that constitutively express CLEC5A or in the lentiviral-transduced stable CHO and CHO-Lec2 cells that overly expressed CLEC5A. To investigate downstream signaling upon engagement of CLEC5A to influenza virus, M-CSF or GM-CSF differentiated human macrophages with high expression levels of CLEC5A and DAP12, a known adaptor protein for CLEC5A upon phosphorylation to initiate signal transduction, was subjected to CLEC5A siRNA gene silencing followed by infection with recombinant A/PR/8/34 virus expressing HA and NA derived from either VN1203 (H5N1) or HK5498 (H1N1) viruses. RG-PR8xVN1203HA,NA (H5N1) exhibited a higher infectivity and induced higher levels of pro-inflammatory cytokines (TNF-( and IFN-α) and chemokines (IP-10, MCP-1, MIG and MIP-1α) secretion in M-CSF or GM-CSF differentiated macrophages while compared to that of the RG-PR8xHK5498HA,NA (H1N1) virus. Knocking-down CLEC5A in macrophages led to a universal reduction of cytokines and chemokines secretion after infection with either the RG-PR8xVN1203HA,NA, RG-PR8xHK5498HA,NA, RG-A/VN/1203/04 (H5N1) or A/Shanghai/2/2014 (H7N9) viruses, suggesting that CLEC5A plays a role as cytokine and chemokine amplifier after influenza infection. Since DAP12 phosphorylation is known to activate downstream signaling via Spleen tyrosine kinase (Syk), pre-incubation of M-CSF macrophages with a Syk inhibitor (Bay 61-3606) also lead to a significant reduction of TNF-α and IP-10 in infected macrophages. A higher mortality was observed in CLEC5A-/- mice while compared to the wild-type C57BL/6 mice after challenged with a lethal dose of RG-A/VN/1203/04 (H5N1) influenza virus suggesting that CLEC5A as a host innate response amplifier play a protective role upon influenza infection. In conclusion, we have identified CLEC5A as a novel host factor for influenza pathogenesis by modulating host innate inflammatory response.
published_or_final_version
Public Health
Doctoral
Doctor of Philosophy
APA, Harvard, Vancouver, ISO, and other styles
8

Gonçalves, Maia Maria João. "Le syndrome Xeroderma Pigmentosum : Un nouveau modèle pour l’étude du rôle des fibroblastes dans la modulation de la réponse immunitaire innée contre les cellules cutanées cancéreuses." Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2019. http://www.theses.fr/2019AZUR4037.

Full text
Abstract:
L’étiologie des cancers cutanées est liée à des mutations génétiques résultant de l’exposition aux rayonnements ultraviolets (UV) émis par le soleil. La propagation des cellules cancéreuses dépend aussi des interactions avec les cellules présentes dans le microenvironnement circulant, notamment des fibroblastes associés au cancer (FAC) et des cellules immunitaires. Xeroderma pigmentosum (XP) est une maladie génétique qui comprend 7 groupes de complémentation génétique (XP-A à XP-G). Les patients XP présentent une déficience du mécanisme de réparation des lésions de l’ADN provoquées par les UV. Ces patients sont susceptibles au développement précoce de très nombreux cancers cutanées. XP-C est le groupe de complémentation le plus représenté en Europe. Chez ces patients, les carcinomes spino-cellularies (CSC) sont plus fréquents que les carcinomes baso-cellulaires (CBC) (taux 5 : 1). Les CSC ont un potentiel métastatique plus élevé que les CBC. Des travaux précédents ont suggéré que la réponse immunitaire chez les patients XP pouvait être altérée, incluant un déficit de l’activité cytolytique des cellules Natural Killer (NK) et une diminution du nombre des lymphocytes T circulants.L’objectif central de cette thèse était, d’identifier des facteurs du microenvironnement impliqués dans la progression des cancer cutanées agressifs, en prenant comme modèle de susceptibilité au cancer, des cellules de patients XP-C. Une analyse transcriptomique comparant les fibroblastes WT et des patients XP-C a permis d’identifier que CLEC2A, un ligand activateur du récepteur NKp65 des cellules NK, est exprimé par les fibroblastes WT mais pas par les fibroblastes XP-C. Nos travaux ont pu montrer une diminution du niveau d’expression de CLEC2A au cours de la sénescence réplicative ; une absence dans les FAC et dans les CSC et que, des facteurs solubles secrétés para les CSC diminuent l’expression de CLEC2A. Ces résultats suggèrent que la perte de CLEC2A peut induire un déficit d’activation des cellules NK au sein du microenvironnement tumoral et dans les dermes des patients XP-C. Par la suite, nous avons élaboré un modèle de culture de peau 3D, dans lequel nous avons introduit des cellules NK, en présence ou absence d’anticorps bloquants CLEC2A. Ce modèle nous a permis de montrer que l’interaction CLEC2A/NKp65 régule l’invasion des CSC via un dialogue entre fibroblastes et cellules NK. Nos résultats suggèrent que l’expression de CLEC2A dans les fibroblastes WT contribue à la surveillance immunitaire dans la peau et que son absence, par des facteurs encore inconnus, favorise le développement des cancers agressifs chez les patients XP-C. CLEC2A peut être une cible dans le combat contre la progression des CSC
Skin cancer etiology is related to genetic mutations arising after ultraviolet (UV) sun exposure. The propagation of cancer cells is also dependent of a crosstalk with cells present in the surrounding microenvironment, mainly cancer associated fibroblasts (CAF) and immune cells. Xeroderma pigmentosum (XP) is a genetic disease that comprises seven groups of genetic complementation (XP-A to XP-G). XP patients present a default in the mechanism responsible for the repair of UV-induced DNA lesions. They are prone to develop skin cancers with high frequencies early in their life. XP-C is the most represented complementation group in Europe and in XP-C patients squamous cell carcinoma (SCC) are more frequent than basal cell carcinoma (BCC) (ratio 5:1). SCC have high metastatic potential compared to BCC. Previous studies suggested that the immune responses in XP patients could be altered with defects in their NK lytic activity and a decrease in the levels of circulating T lymphocytes. The main objective of this thesis was to identify microenvironment factors that could contribute to the progression of aggressive skin cancers using XP-C disease cells as a model of skin cancer susceptibility. Comparative transcriptomic analysis of WT and XP-C dermal patient’s fibroblasts revealed that CLEC2A, a ligand of the activating NK receptor NKp65 implicated in the activation of the innate immune system, is expressed in WT fibroblasts and absent in XP-C fibroblasts. Additional work showed that CLEC2A level is decreased in WT fibroblasts during replicative senescence, is absent in CAF and SCC, and is down regulated by soluble factors secreted by SCC cells. These results suggest that the loss of CLEC2A may induce a deficit of NK cell activation in the tumor microenvironment of SCC and in the dermis of XP-C patients. Elaboration of 3D skin culture models including NK cells and, in the presence or absence of blocking anti-CLEC2A antibody, allowed us to show that CLEC2A/NKp65 interaction regulates SCC cells invasion through a crosstalk between fibroblasts and NK cells. Our results suggest that the expression of CLEC2A in fibroblasts contributes to skin immune surveillance while, conversely, its absence under yet unidentified factors, favors the development of aggressive cancers in XP-C patients. CLEC2A could be a potential target in the fight against SCC progression
APA, Harvard, Vancouver, ISO, and other styles
9

Medina, Mendieta Clelia [Verfasser]. "Business-to-Consumer eCommerce Adoption in Nicaragua / Clelia Medina Mendieta." Berlin : Freie Universität Berlin, 2018. http://d-nb.info/1170814581/34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Khan, Kabir Ali. "Investigating the extracellular interactions of the tumour endothelial marker CLEC14A." Thesis, University of Birmingham, 2016. http://etheses.bham.ac.uk//id/eprint/6909/.

Full text
Abstract:
CLEC14A is an endothelial specific type I transmembrane glycoprotein, which is highly expressed on the vasculature of a wide range of different solid tumours. Identifying extracellular interactions of CLEC14A holds promise for new targets in anti-angiogenic strategies for cancer treatment. CLEC14A directly binds to the extracellular matrix protein multimerin-2 (MMRN2). Both proteins are upregulated with tumour progression and are implicated in endothelial cell function. The CLEC14A-MMRN2 interaction occurs when both proteins are expressed at endogenous levels in endothelial cells, and is dependent upon the C-type lectin domain of CLEC14A. Blocking the CLEC14A-MMRN2 interaction had anti-angiogenic effects and could inhibit the growth of mouse tumour models. Finally, the localisation and targeting of CLEC14A was investigated in vivo by use of humanised antibodies and antibody drug conjugates. Data presented in this thesis reinforce the pro-angiogenic functions of CLEC14A and the likelihood of it being a good target for cancer therapy.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Clec9A"

1

Berti, Paolo. Santa Clelia Barbieri. Milano: Edizioni paoline, 1991.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Bassini, Remo. Dicono di Clelia. Milano: Mursia, 2006.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Ebenezer, Lyn. Clecs Cwmderi. Caerydd: Hughes a'i Fab, 1986.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Podestá, Clelia. Mi nombre es Clelia. [Santiago de Chile: Editorial Los Heroes, 1996.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Boston, Credit Suisse First. Telecom services: CLECS. London: Credit Suisse First Boston, 2000.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Durrell, Lawrence. Clea. Thorndike, Me: G.K. Hall & Co., 2000.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Lawrence, Durrell. Clea. New York: Penguin Books, 1991.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Clelia Farnese: La figlia del Gran Cardinale. Viterbo: Sette città, 2010.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Vatteroni, Sergio. Falsa clercia: La poesia anticlericale dei trovatori. Alessandria: Edizioni dell'Orso, 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Vatteroni, Sergio. Falsa clercia: La poesia anticlericale dei trovatori. Alessandria: Edizioni dell'Orso, 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Clec9A"

1

Tetlak, Piotr, and Christiane Ruedl. "Analysis of Dendritic Cell Function Using Clec9A-DTR Transgenic Mice." In Methods in Molecular Biology, 275–89. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3606-9_20.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Reschen, Michael E., and Christopher A. O’Callaghan. "CLEC5A." In Encyclopedia of Signaling Molecules, 1147–54. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_572.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Willment, Janet A., and Gordon D. Brown. "CLEC7A." In Encyclopedia of Signaling Molecules, 1154–61. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_584.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Reschen, Michael, and Christopher A. O’Callaghan. "CLEC5A." In Encyclopedia of Signaling Molecules, 1–8. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_572-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "Clec1a." In Encyclopedia of Signaling Molecules, 412. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100278.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "CLEC5A." In Encyclopedia of Signaling Molecules, 421–25. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_572.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "CLEC7A." In Encyclopedia of Signaling Molecules, 425–31. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_584.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Reschen, Michael E., Anita R. Mistry, and Christopher A. O’Callaghan. "CLEC4E." In Encyclopedia of Signaling Molecules, 1138–47. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_571.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Reschen, Michael E., Anita R. Mistry, and Christopher A. O’Callaghan. "CLEC4E." In Encyclopedia of Signaling Molecules, 1–9. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_571-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Knudsen, Lars R. "CLEFIA." In Encyclopedia of Cryptography and Security, 210–11. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4419-5906-5_561.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Clec9A"

1

Radford, Kristen, Frances Pearson, Kelly-Anne Masterman, Kirsteen Tullett, Oscar Haigh, Carina Walpole, Ghazal Daraj, Ingrid Leal Rojas, and Mireille Lahoud. "Abstract B125: Targeting human CD141+ DC using CLEC9A antibodies for cancer immunotherapy." 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-b125.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Etemad, M., G. Rink, C. Gerhards, and P. Bugert. "Correlation of CLEC1B Gene Polymorphisms with Plasma Levels of Soluble CLEC-2 in Healthy Individuals." In 63rd Annual Meeting of the Society of Thrombosis and Haemostasis Research. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1680198.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Ahmadi, Siavash, Mahshid Delavar, Javad Mohajeri, and Mohammad Reza Aref. "Security analysis of CLEFIA-128." In 2014 11th International ISC Conference on Information Security and Cryptology (ISCISC). IEEE, 2014. http://dx.doi.org/10.1109/iscisc.2014.6994027.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Proenca, Paulo, and Ricardo Chaves. "Compact CLEFIA Implementation on FPGAS." In 2011 International Conference on Field Programmable Logic and Applications (FPL). IEEE, 2011. http://dx.doi.org/10.1109/fpl.2011.101.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Machado, Thiago, Alanna Santos, Tamiris Barros, Patrícia Oliveira, and Ana Bom. "High CLEC5A expression on monocytes is related with severe COVID-19." In International Symposium on Immunobiologicals. Instituto de Tecnologia em Imunobiológicos, 2022. http://dx.doi.org/10.35259/isi.2022_52201.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Takahashi, Junko, and Toshinori Fukunaga. "Improved Differential Fault Analysis on CLEFIA." In 2008 5th Workshop on Fault Diagnosis and Tolerance in Cryptography (FDTC). IEEE, 2008. http://dx.doi.org/10.1109/fdtc.2008.14.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Ali, Sk Subidh, and Debdeep Mukhopadhyay. "Improved Differential Fault Analysis of CLEFIA." In 2013 Workshop on Fault Diagnosis and Tolerance in Cryptography (FDTC). IEEE, 2013. http://dx.doi.org/10.1109/fdtc.2013.11.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Bittencourt, Joao Carlos, Joao Carlos Resende, Wagner Luiz de Oliveira, and Ricardo Chaves. "CLEFIA Implementation with Full Key Expansion." In 2015 Euromicro Conference on Digital System Design (DSD). IEEE, 2015. http://dx.doi.org/10.1109/dsd.2015.55.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Tsunoo, Yukiyasu, Etsuko Tsujihara, Maki Shigeri, Tomoyasu Suzaki, and Takeshi Kawabata. "Cryptanalysis of CLEFIA using multiple impossible differentials." In 2008 International Symposium on Information Theory and Its Applications (ISITA). IEEE, 2008. http://dx.doi.org/10.1109/isita.2008.4895639.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Cheltha C., Jeba Nega, Rajan Kumar Jha, Mohit Jain, and Prahlad Kumar Sharma. "Contemporary Encryption Technique for Images using CLEFIA." In 2018 Second International Conference on Computing Methodologies and Communication (ICCMC). IEEE, 2018. http://dx.doi.org/10.1109/iccmc.2018.8488153.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Clec9A"

1

Katagi, M., and S. Moriai. The 128-Bit Blockcipher CLEFIA. RFC Editor, March 2011. http://dx.doi.org/10.17487/rfc6114.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Fish, Jim. Overture to CLEA : the closed loop efficiency analysis project. Office of Scientific and Technical Information (OSTI), April 1985. http://dx.doi.org/10.2172/1574617.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Hawn, D., and J. Fish. CLEA: the Closed Loop Efficiency Analysis Facility for thermochemical energy transport studies. Office of Scientific and Technical Information (OSTI), May 1986. http://dx.doi.org/10.2172/5712175.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Clec9A' for particular source types:
Journal articles Dissertations / Theses Books
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!

To the bibliography