Relevant bibliographies by topics / CLEC2A

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Academic literature on the topic 'CLEC2A'

Author: Grafiati
Published: 4 June 2021
Last updated: 2 February 2022

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Journal articles on the topic "CLEC2A"

1

Spreu, Jessica, Eike C. Kienle, Birgit Schrage, and Alexander Steinle. "CLEC2A: a novel, alternatively spliced and skin-associated member of the NKC-encoded AICL–CD69–LLT1 family." Immunogenetics 59, no. 12 (November 29, 2007): 903–12. http://dx.doi.org/10.1007/s00251-007-0263-1.

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Gonçalves-Maia, Maria, Yannick Gache, Miguel Basante, Estelle Cosson, Emie Salavagione, Margot Muller, Françoise Bernerd, et al. "NK Cell and Fibroblast-Mediated Regulation of Skin Squamous Cell Carcinoma Invasion by CLEC2A Is Compromised in Xeroderma Pigmentosum." Journal of Investigative Dermatology 140, no. 9 (September 2020): 1723–32. http://dx.doi.org/10.1016/j.jid.2020.01.021.

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Elleisy, Nagi, Sarah Rohde, Astrid Huth, Nicole Gittel, Änne Glass, Steffen Möller, Georg Lamprecht, Holger Schäffler, and Robert Jaster. "Genetic association analysis of CLEC5A and CLEC7A gene single-nucleotide polymorphisms and Crohn’s disease." World Journal of Gastroenterology 26, no. 18 (May 14, 2020): 2194–202. http://dx.doi.org/10.3748/wjg.v26.i18.2194.

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Araúzo-Bravo, Marcos J., Denis Delic, Daniela Gerovska, and Frank Wunderlich. "Protective Vaccination Reshapes Hepatic Response to Blood-Stage Malaria of Genes Preferentially Expressed by NK Cells." Vaccines 8, no. 4 (November 13, 2020): 677. http://dx.doi.org/10.3390/vaccines8040677.

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The role of natural killer (NK) cells in the liver as first-line post infectionem (p.i.) effectors against blood-stage malaria and their responsiveness to protective vaccination is poorly understood. Here, we investigate the effect of vaccination on NK cell-associated genes induced in the liver by blood-stage malaria of Plasmodium chabaudi. Female Balb/c mice were vaccinated at weeks 3 and 1 before being infected with 106P. chabaudi-parasitized erythrocytes. Genes preferentially expressed by NK cells were investigated in livers of vaccination-protected and non-protected mice on days 0, 1, 4, 8, and 11 p.i. using microarrays, qRT-PCR, and chromosome landscape analysis. Blood-stage malaria induces expression of specific genes in the liver at different phases of infection, i.e., Itga1 in expanding liver-resident NK (lrNK) cells, Itga2 in immigrating conventional NK (cNK) cells; Eomes and Tbx21 encoding transcription factors; Ncr1, Tnfsf10, Prf1, Gzma, Gzmb, Gzmc, Gzmm, and Gzmk encoding cytolytic effectors; natural killer gene complex (NKC)-localized genes encoding the NK cell receptors KLRG1, KLRK1, KLRAs1, 2, 5, 7, KLRD1, KLRC1, KLRC3, as well as the three receptors KLRB1A, KLRB1C, KLRB1F and their potential ligands CLEC2D and CLEC2I. Vaccination enhances this malaria-induced expression of genes, but impairs Gzmm expression, accelerates decline of Tnfsf10 and Clec2d expression, whereas it accelerates increased expression of Clec2i, taking a very similar time course as that of genes encoding plasma membrane proteins of erythroblasts, whose malaria-induced extramedullary generation in the liver is known to be accelerated by vaccination. Collectively, vaccination reshapes the response of the liver NK cell compartment to blood-stage malaria. Particularly, the malaria-induced expansion of lrNK cells peaking on day 4 p.i. is highly significantly (p < 0.0001) reduced by enhanced immigration of peripheral cNK cells, and KLRB1F:CLEC2I interactions between NK cells and erythroid cells facilitate extramedullary erythroblastosis in the liver, thus critically contributing to vaccination-induced survival of otherwise lethal blood-stage malaria of P. chabaudi.
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Macri, Christophe, Claire Dumont, Scott Panozza, Mireille H. Lahoud, Irina Caminschi, Jose A. Villadangos, Angus P. R. Johnston, and Justine D. Mintern. "Antibody-mediated targeting of antigen to C-type lectin-like receptors Clec9A and Clec12A elicits different vaccination outcomes." Molecular Immunology 81 (January 2017): 143–50. http://dx.doi.org/10.1016/j.molimm.2016.12.010.

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Vitry, Julien, Guillaume Paré, Andréa Murru, Xavier Charest-Morin, Halim Maaroufi, Kenneth R. McLeish, Paul H. Naccache, and Maria J. Fernandes. "Regulation of the Expression, Oligomerisation and Signaling of the Inhibitory Receptor CLEC12A by Cysteine Residues in the Stalk Region." International Journal of Molecular Sciences 22, no. 19 (September 22, 2021): 10207. http://dx.doi.org/10.3390/ijms221910207.

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CLEC12A is a myeloid inhibitory receptor that negatively regulates inflammation in mouse models of autoimmune and autoinflammatory arthritis. Reduced CLEC12A expression enhances myeloid cell activation and inflammation in CLEC12A knock-out mice with collagen antibody-induced or gout-like arthritis. Similarly to other C-type lectin receptors, CLEC12A harbours a stalk domain between its ligand binding and transmembrane domains. While it is presumed that the cysteines in the stalk domain have multimerisation properties, their role in CLEC12A expression and/or signaling remain unknown. We thus used site-directed mutagenesis to determine whether the stalk domain cysteines play a role in CLEC12A expression, internalisation, oligomerisation, and/or signaling. Mutation of C118 blocks CLEC12A transport through the secretory pathway diminishing its cell-surface expression. In contrast, mutating C130 does not affect CLEC12A cell-surface expression but increases its oligomerisation, inducing ligand-independent phosphorylation of the receptor. Moreover, we provide evidence that CLEC12A dimerisation is regulated in a redox-dependent manner. We also show that antibody-induced CLEC12A cross-linking induces flotillin oligomerisation in insoluble membrane domains in which CLEC12A signals. Taken together, these data indicate that the stalk cysteines in CLEC12A differentially modulate this inhibitory receptor’s expression, oligomerisation and signaling, suggestive of the regulation of CLEC12A in a redox-dependent manner during inflammation.
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Kenderian, Saad S., Marco Ruella, Olga Shestova, Michael Klichinsky, Miriam Y. Kim, Craig Soderquist, Adam Bagg, et al. "Leukemia Stem Cells Are Characterized By CLEC12A Expression and Chemotherapy Refractoriness That Can be Overcome By Targeting with Chimeric Antigen Receptor T Cells." Blood 128, no. 22 (December 2, 2016): 766. http://dx.doi.org/10.1182/blood.v128.22.766.766.

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Abstract Chemo-refractory acute myeloid leukemia (AML) is associated with poor prognosis and treatment options are extremely limited. Most of these patients are ineligible for allogeneic stem cell transplantation. Chemo-refractory AML is thought to arise due to selection pressure of resistant clones from prior use of chemotherapy or in some cases pre-exist due to properties of the leukemic stem cells (LSC). CLEC12A (also known as CLL1) has previously been described as being selectively over expressed in LSCs. Successful modalities to target CLEC12A and eradicate the LSC would overcome chemo-refractoriness in AML and would represent a vertical advance in the field. In this study, we confirm that CLEC12A is heterogenously expressed on AML blasts and over-expressed on AML LSC. We also show that CLEC12A is overexpressed on bone marrows from patients with AML that fail to achieve a complete remission after induction chemotherapy, suggesting that it could be a marker for residual disease that is refractory to chemotherapy. We then separated AML blasts into CLEC12A positive or negative cells by magnetic sorting. CLEC12A positive blasts selected from AML patients were more resistant to chemotherapy compared to CLEC12A negative blasts (20% killing of CLEC12A positive AML cells versus 43% of CLEC12A negative AML cells when cultured with cytarabine 10 µg/ml, P=0.01). This finding was confirmed by using the AML MOLM14 cell line engineered to overexpress CLEC12A. CLEC12Ahigh MOLM14 cells were more resistant to chemotherapy compared to wild type MOLM14 cells (P=0.003). We then evaluated CLEC12A resistance to chemotherapy in a patient derived AML xenograft model. We found a relative increase in CLEC12A positive cells post Ara-C induction chemotherapy in AML xenograft models (Figure 1). The observation that CLEC12A positive cells are more resistant to chemotherapy provided a solid rationale to target CLEC12A with chimeric antigen receptor T (CART) cells. We therefore developed a second generation CLEC12A directed CAR construct using CD3z and 41BB costimulatory domains and generated CLEC12A CART cells by lentiviral transduction with this construct. Upon incubation with primary AML samples or AML cell lines, CLEC12A CART cells resulted in modest effector functions, due to the heterogeneity of CLEC12A expression on AML blasts. However when CLEC12A overexpressed MOLM14 cell line or CLEC12Apos selected leukemic cells were used as targets, CLEC12A-CART cells resulted in potent cytotoxicity, proliferation and cytokine production, indicating that CLEC12A-CART cells are more specific for LSC. To test the in vivo anti-leukemic activity of CLEC12A CARTs, we used primary human AML blasts xenografted into NSG-S mice (NOD-SCID-γc-/-, additionally transgenic for human stem cell factor, IL3 and GM-CSF). Treatment with CLEC12A CART (single dose, 1x105 total T cells via tail vein injection) resulted in modest activity against AML when employed as monotherapy. To investigate the potential role of CLEC12A CART cells in eradication of MRD and LSC, mice were treated first with chemotherapy (cytarabine 60 mg/kg intraperitoneal injection daily for 5 days) followed by a single dose (1x105 total T cells via tail vein injection) of either CLEC12A CARTs or control untransduced T cells (UTD). Treatment with CLEC12A CART cells resulted in eradication of leukemia and prolonged survival in these mice (overall survival at 200 days of 100% after CLEC12A CARTs compared to 20% after UTD, p=0.01, Figure 2). In conclusion, our preclinical studies reveal that CLEC12A positive cells in leukemia are resistant to chemotherapy and can be successfully targeted with CART cells. CLEC12A CART cells can potentially be employed as a consolidation regimen after induction chemotherapy to eradicate LSC and MRD in AML. Disclosures Kenderian: Novartis: Patents & Royalties, Research Funding. Ruella:novartis: Patents & Royalties: Novartis, Research Funding. Singh:Novartis: Employment. Richardson:Novartis: Employment, Patents & Royalties, Research Funding. June:Tmunity: Equity Ownership, Other: Founder, stockholder ; Immune Design: Consultancy, Equity Ownership; Novartis: Honoraria, Patents & Royalties: Immunology, Research Funding; University of Pennsylvania: Patents & Royalties; Celldex: Consultancy, Equity Ownership; Johnson & Johnson: Research Funding; Pfizer: Honoraria. Gill:Novartis: Patents & Royalties, Research Funding.
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Chen, Po-Ku, Shie-Liang Hsieh, Joung-Liang Lan, Chi-Chen Lin, Shih-Hsin Chang, and Der-Yuan Chen. "Elevated Expression of C-Type Lectin Domain Family 5-Member A (CLEC5A) and Its Relation to Inflammatory Parameters and Disease Course in Adult-Onset Still’s Disease." Journal of Immunology Research 2020 (April 23, 2020): 1–11. http://dx.doi.org/10.1155/2020/9473497.

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C-type lectin domain family 5-member A (CLEC5A) associates with adaptor DAP12 (DNAX activation protein 12) to form receptor complexes involved in inflammatory responses. We postulated a potential role of CLEC5A in the pathogenesis of adult-onset Still’s disease (AOSD) and aimed to investigate CLEC5A expression and its association with activity parameters and disease course. In 34 AOSD patients and 12 healthy controls (HC), circulating levels of CLEC5A-expressing monocytes or granulocytes were determined by flow cytometry analysis, the mRNA expression of CLEC5A and DAP12 on PBMCs by quantitative PCR, and plasma levels of proinflammatory cytokines by ELISA. AOSD patients had significantly higher percentages and mean fluorescence intensity (MFI) of CLEC5A-expressing monocytes (median 62.1% and 3.20, respectively) or granulocytes (72.6% and 3.22, respectively) compared with HC (in monocytes: 17.0% and 0.65, both p<0.001; in granulocytes: 67.3%, p<0.05 and 0.90, p<0.001; respectively). Patients also had significantly higher levels of CLEC5A mRNA expression on PBMCs compared with HC (median 1.77 vs. 0.68, p<0.05). The levels of CLEC5A-expressing monocytes or granulocytes were positively associated with activity scores and levels of IL-1β and IL-18 in AOSD patients. The patients with a systemic pattern had significantly higher levels of CLEC5A-expressing granulocytes and IL-18 compared to those with a chronic articular pattern of disease course. After 6 months of therapy, levels of CLEC5A-expressing monocytes and granulocytes significantly declined, paralleling the decrease of AOSD activity. Elevated CLEC5A levels and their positive association with activity parameters suggest that CLEC5A is involved in the pathogenesis and may serve as an activity indicator of AOSD.
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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.

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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.
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Kan, Hung-Wei, Chin-Hong Chang, Ying-Shuang Chang, Yi-Ting Ko, and Yu-Lin Hsieh. "Genetic loss-of-function of activating transcription factor 3 but not C-type lectin member 5A prevents diabetic peripheral neuropathy." Laboratory Investigation 101, no. 10 (June 25, 2021): 1341–52. http://dx.doi.org/10.1038/s41374-021-00630-5.

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AbstractWe investigated the mediating roles of activating transcription factor 3 (ATF3), an injury marker, or C-type lectin member 5A (CLEC5A), an inflammatory response molecule, in the induction of endoplasmic reticulum (ER) stress and neuroinflammation in diabetic peripheral neuropathy in ATF3 and CLEC5A genetic knockout (aft3−/− and clec5a−/−, respectively) mice. ATF3 was expressed intranuclearly and was upregulated in mice with diabetic peripheral neuropathy (DN) and clec5a−/− mice. The DN and clec5a−/− groups also exhibited neuropathic behavior, but not in the aft3−/− group. The upregulation profiles of cytoplasmic polyadenylation element-binding protein, a protein translation–regulating molecule, and the ER stress-related molecules of inositol-requiring enzyme 1α and phosphorylated eukaryotic initiation factor 2α in the DN and clec5a−/− groups were correlated with neuropathic behavior. Ultrastructural evidence confirmed ER stress induction and neuroinflammation, including microglial enlargement and proinflammatory cytokine release, in the DN and clec5a−/− mice. By contrast, the induction of ER stress and neuroinflammation did not occur in the aft3−/− mice. Furthermore, the mRNA of reactive oxygen species–removing enzymes such as superoxide dismutase, heme oxygenase-1, and catalase were downregulated in the DN and clec5a−/− groups but were not changed in the aft3−/− group. Taken together, the results indicate that intraneuronal ATF3, but not CLEC5A, mediates the induction of ER stress and neuroinflammation associated with diabetic neuropathy.
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Dissertations / Theses on the topic "CLEC2A"

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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.

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

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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
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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/.

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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.
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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.

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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.

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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.

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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.
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Public Health
Doctoral
Doctor of Philosophy
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7

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/.

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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.
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Sormani, Laura. "Identification d’un nouveau gène dans la pigmentation cutanée - CLEC12B." Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2019. http://theses.univ-cotedazur.fr/2019AZUR6037.

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La mélanogenèse est un processus complexe et étroitement régulé. Une étude transcriptomique à large échelle a été réalisée sur des peaux lésionnelles de patients atteints de vitiligo (dépourvues de mélanocytes et donc de pigmentation) comparées à des peaux non lésionnelles et des peaux de sujets sains. L’analyse différentielle des transcrits a permis la découverte d’un nouveau gène dont l’expression est significativement régulée négativement, dans les peaux lésionnelles, en comparaison avec les peaux non lésionnelles ou saines : CLEC12B. Le degré de régulation de CLEC12B était similaire à ceux observés pour les enzymes clefs de la mélanogenèse (TYR, TYRP1 ou DCT) suggérant que CLEC12B pourrait être un gène mélanocytaire important et jouer un rôle, jusqu’ici inconnu, dans la pigmentation cutanée. CLEC12B est membre de la famille des lectines de type C, qui sont des récepteurs transmembranaires possédant un domaine ITIM capable de recruter et d’activer SHP1 et SHP2. Ces phosphatases régulent de nombreuses voies de signalisation cellulaire impliquées dans des processus biologiques importants. À ce jour, très peu de données sont disponibles dans la littérature concernant CLEC12B qui a uniquement été rapporté dans les cellules myéloïdes. Son ligand, ainsi que les voies de signalisation en aval, n’ont toujours pas été identifiés et aucun lien n’a été rapporté entre CLEC12B et la pigmentation cutanée. Nous avons montré, pour la première fois, que CLEC12B est exprimé par les mélanocytes humains normaux (NHM) et que son expression dépend du phototype de la peau. La modulation de l’expression de CLEC12B par shRNA induit une augmentation significative de la production de mélanines dans les NHMs. Au contraire, la surexpression de CLEC12B entraîne une diminution significative de la pigmentation. Ces résultats ont été confirmés à l'aide d'un modèle d'épiderme humain reconstruit. L’utilisation d’un mutant du domaine ITIM de CLEC12B nous a permis de montrer que CLEC12B recrute et active directement les phosphatases SHP1 et SHP2 dans les mélanocytes. Ceci conduit à la régulation négative des facteurs de transcription CREB et MITF ainsi que des enzymes de la mélanogenèse (TYR, TYRP1 et DCT).Ce nouvel apport dans la compréhension de la physiologie de la pigmentation cutanée pourrait permettre, in fine, à l’identification de nouvelles cibles thérapeutiques et aboutir un jour au développement d’agents dans le traitement clinique et cosmétique des troubles pigmentaires
Melanogenesis is a complex and tightly regulated process. A transcriptome analysis in lesional and non-lesional skin of vitligo patients compared to healthy controls allowed us to identify a new gene CLEC12B, which is only expressed in controls and in non lesional skin of vitiligo patients. The decreased expression of CLEC12B in lesional skin of vitiligo patients is comparable to the one observed for key melanocytic genes such as TYR, TYRP1 or DCT suggesting that CLEC12B could be an important melanocytic gene. CLEC12B is a member of the C-type lectin family, which are transmembrane receptors that possess an ITIM domain which can recruit phosphatases. So far, only few data are available on this gene that is essentially reported in myeloid cells. Ligand and downstream signaling of CLEC12B are unknown and to date, no link has been reported between CLEC12B and pigmentation. We demonstrated that CLEC12B is selectively expressed in melanocytes, and that its expression is decreased in highly pigmented skin compared to white skin. Silencing of CLEC12B in normal human melanocytes (NHM) by short hairpin RNA induced a significant increase in melanin production. On the contrary, CLEC12B overexpression using lentiviral vector resulted in significant loss of pigmentation in NHM. These results were confirmed using a reconstructed human epidermis model. Using a mutant of the ITIM domain of CLEC12B, we showed that CLEC12B directly recruits and activate SHP2, leading to the negative regulation of CREB, MITF and melanogenesis enzymes such as tyrosinase and DCT accordingly to the pigmentary phenotypes observed. These results provide novel insights not only for the development of melanogenic agents in the clinical and cosmetic fields, but also for a better understanding of the melanocyte biology and regulation of melanogenesis
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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.

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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)
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10

Montaudié, Henri. "CLEC12B un gène de la famille des lectines impliqué dans le processus de melanomagénèse en agissant comme un gène suppresseur de tumeurs : CLEC12B un gène suppresseur de tumeurs impliqué dans le mélanome." Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2019. http://www.theses.fr/2019AZUR6013.

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Malgré les progrès thérapeutiques importants accomplis ces dernières années, le mélanome garde un pronostic péjoratif au stade métastatique. Il est donc essentiel d’explorer les mécanismes moléculaires et cellulaires impliqués dans le processus de mélanomagénèse dans la perspective de découvrir de nouvelles cibles thérapeutiques.Une analyse transcriptomique comparative de la peau de patients atteints de vitiligo (et donc dénuée de mélanocytes) par rapport à de la peau non lésionnelle et la peau de sujets témoins, nous a permis de découvrir que le récepteur de la lectine C, CLEC12B (C-type lectin domain family 12-member B) était sélectivement et fortement exprimé par les mélanocytes. L'objectif de cette étude était d'étudier le rôle de CLEC12B in vitro et in vivo dans le mélanome. Nous avons d’abord montré que l’expression des transcrits de CLEC12B, par technique RT-PCR, était plus faible dans les lignées cellulaires de mélanome et dans les cellules de mélanome extraites de métastases de patients que dans les mélanocytes humains normaux. D’autre part, l'analyse protéique par immunohistochimie a montré une expression plus faible de CLEC12B, dans des échantillons de mélanome humain (mélanomes primaires et métastatiques de patients) par rapport aux nævi. La base de données TCGA, a révélé que les patients avec une expression élevée de CLEC12B avaient une survie médiane significativement supérieure à ceux avec une expression faible. Ces premiers résultats suggèrent un rôle potentiel de CLEC12B dans le processus de mélanomagénèse. Dans un second temps, en utilisant une construction de lentivirus, nous avons surexprimé (Ov-CLEC12B) et régulé négativement (Sh-CLEC12B) CLEC12B dans deux lignées cellulaires de mélanome humain (A375 BRAF muté et MeWo BRAF sauvage). Ainsi nous avons démontré que Ov-CLEC12B inhibait la prolifération et la formation de colonies, par l’activation de p53/p21/p27 et l’inhibition des STATs et notamment STAT3 qui est constitutivement activé dans le mélanome. Par ailleurs, par une expérience de co-immunoprécipitation et après avoir généré un mutant de CLEC12B sur son domaine ITIM, nous avons montré que CLEC12B par son domaine ITIM, recrute et active directement la tyrosine phosphatase SHP-2. Une fois activée par CLEC12B, SHP-2 inactive la voie STAT (diminution des formes phosphorylées de STAT1, 3 et 5) et augmente l’expression de p53/p21/p27 entrainant un ralentissement du cycle cellulaire en phase G0-G1. Des effets opposés sont observés après l’extinction de CLEC12B. Enfin, les propriétés tumorigèniques de CLEC12B ont été étudiées chez des souris nude avec des expériences de xénogreffe de tumeur (injection de la lignée A375 Ov et Sh-CLEC12B). En accord avec les résultats in vitro, la croissance tumorale dans le groupe Ov-CLEC12B était significativement réduite par rapport au groupe véhicule et était associée à une diminution de l'expression de pSTAT3 et à une augmentation de p53 dans les tumeurs. Le contraire a été observé dans les conditions Sh-CLEC12B.Au total, ce travail révèle que CLEC12B est un nouveau gène suppresseur du mélanome qui agit en régulant le cycle cellulaire et en réprimant l'activation de STAT
Despite significant progress in recent years, melanoma remains among the most aggressive and deadly human cancers. Thus, it still remains essential to explore the molecular and cellular mechanisms involved in the melanomagenesis process in order to discover new therapeutic options. A transcriptomic analysis from vitiligo patient skins allowed us to discover that the C-lectin receptor CLEC12B (C-type lectin domain family 12-member B) is selectively and strongly expressed by melanocytes. The objective of this study was to investigate the role of CLEC12B in melanoma. We first showed that the expression of CLEC12B is lower in melanoma cell lines, and in melanoma cells extracted from patient metastases, compared to the expression in normal human melanocytes. Immunohistochemical analysis further showed a lower expression of CLEC12B, in human melanoma samples (primary and metastatic melanomas from patients) compared to melanocytic nevi. Using the TCGA database, we found that patients with high CLEC12B expression have a significantly higher median survival than those with low expression. Taken together, these first results suggested a potential role of CLEC12B in melanomagenesis process. Subsequently, using a lentivirus construct, we overexpressed (Ov-CLEC12B) and downregulated (Sh-CLEC12B) CLEC12B in human melanoma cells lines, and we demonstrated that CLEC12B inhibits the proliferation and colony formation, through activation of p53/p21/p27 and the inhibition of STAT pathway. We demonstrated, using a co-immunoprecipitation assay, and after generating a mutant of CLEC12B ITIM domain, that CLEC12B function is mediated by its ITM domain, which directly recruits and activates the tyrosine phosphatase SHP-2. Once activated by CLEC12B, SHP-2 inactivates the STAT pathway, as observed with a decrease of STAT1, STAT3 and STAT5 phosphorylated forms and promotes p53/p21/p27 pathway activation with a slow down in G0-G1 phase of cell cycle. Opposite effects were observed after silencing CLEC12B. Finally, tumorigenic properties of CLEC12B were analyzed in nude mice with tumor xenograft experiments. In accordance with in vitro results, the tumor growth in Ov CLEC12B group was significantly decreased compared to vehicle group and was associated with a decreased expression of pSTAT3 and an increase of p53 within the tumors. The opposite was noted with Sh CLEC12B. This study reveals CLEC12B as a novel potent suppressor gene in melanoma by regulating cell cycle and repressing STAT activation
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Books on the topic "CLEC2A"

1

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

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

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

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

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

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

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

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

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

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

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Book chapters on the topic "CLEC2A"

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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.

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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.

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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.

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "CLEC2B." In Encyclopedia of Signaling Molecules, 416. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100284.

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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.

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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.

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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.

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "Clec2." In Encyclopedia of Signaling Molecules, 413. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100281.

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "CLEC4E." In Encyclopedia of Signaling Molecules, 416–21. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_571.

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "Clec1b." In Encyclopedia of Signaling Molecules, 413. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100279.

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Conference papers on the topic "CLEC2A"

1

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.

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Guadagnuolo, Viviana, Enrica Imbrogno, Andrea Ghelli Luserna di Rorà, Antonella Padella, Giorgia Simonetti, Emanuela Ottaviani, Cristina Papayannidis, et al. "Abstract 3886: Clec12a: A new AML stem cell-associated antigen." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3886.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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Reports on the topic "CLEC2A"

1

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

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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.

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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.

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