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Добірка наукової літератури з теми "CLEC4C"

Автор: Grafiati

Опубліковано: 11 березня 2023

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Статті в журналах з теми "CLEC4C"

Riboldi, Elena, Roberta Daniele, Carmen Parola, Antonio Inforzato, Phoebe L. Arnold, Daniela Bosisio, Daved H. Fremont, Antonio Bastone, Marco Colonna, and Silvano Sozzani. "Human C-type Lectin Domain Family 4, Member C (CLEC4C/BDCA-2/CD303) Is a Receptor for Asialo-galactosyl-oligosaccharides." Journal of Biological Chemistry 286, no. 41 (August 31, 2011): 35329–33. http://dx.doi.org/10.1074/jbc.c111.290494.

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Plasmacytoid dendritic cells are specialized in the production of type I interferon (type I IFN), which promotes antiviral and antitumor responses, as well as autoimmune disorders. Activation of type I IFN secretion depends on the pattern recognition receptors TLR7 and TLR9, which sense microbial RNA and DNA, respectively. Type I IFN production is modulated by several receptors, including the type II C-type lectin domain family 4, member C (CLEC4C). The natural ligand of CLEC4C is unknown. To identify it, here we probed a glycan array with a soluble form of the CLEC4C ectodomain. We found that CLEC4C recognizes complex type sugars with terminal galactose. Importantly, soluble CLEC4C bound peripheral blood leukocytes and tumor cells that express glycans with galactose residues at the non-reducing ends. The positive and negative modulation of galactose residues on cell membranes was paralleled by the regulation of type I IFN secretion by plasmacytoid dendritic cells in co-culture experiments in vitro. These results suggest that the modulation in the expression of non-sialylated oligosaccharides by invading pathogens or transformed cells may affect type I IFN response and immune surveillance.

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Miller, Hannah L., Prabhakar Sairam Andhey, Melissa K. Swiecki, Bruce A. Rosa, Konstantin Zaitsev, Alexandra-Chloe Villani, Makedonka Mitreva, et al. "Altered ratio of dendritic cell subsets in skin-draining lymph nodes promotes Th2-driven contact hypersensitivity." Proceedings of the National Academy of Sciences 118, no. 3 (January 11, 2021): e2021364118. http://dx.doi.org/10.1073/pnas.2021364118.

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Plasmacytoid dendritic cells (pDCs) specialize in the production of type I IFN (IFN-I). pDCs can be depleted in vivo by injecting diphtheria toxin (DT) in a mouse in which pDCs express a diphtheria toxin receptor (DTR) transgene driven by the human CLEC4C promoter. This promoter is enriched for binding sites for TCF4, a transcription factor that promotes pDC differentiation and expression of pDC markers, including CLEC4C. Here, we found that injection of DT in CLEC4C-DTR+mice markedly augmented Th2-dependent skin inflammation in a model of contact hypersensitivity (CHS) induced by the hapten fluorescein isothiocyanate. Unexpectedly, this biased Th2 response was independent of reduced IFN-I accompanying pDC depletion. In fact, DT treatment altered the representation of conventional dendritic cells (cDCs) in the skin-draining lymph nodes during the sensitization phase of CHS; there were fewer Th1-priming CD326+CD103+cDC1 and more Th2-priming CD11b+cDC2. Single-cell RNA-sequencing of CLEC4C-DTR+cDCs revealed that CD326+DCs, like pDCs, expressed DTR and were depleted together with pDCs by DT treatment. Since CD326+DCs did not expressTcf4, DTR expression might be driven by yet-undefined transcription factors activating the CLEC4C promoter. These results demonstrate that altered DC representation in the skin-draining lymph nodes during sensitization to allergens can cause Th2-driven CHS.

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Murray, Liisa, Yang Xi, and John W. Upham. "CLEC4C gene expression can be used to quantify circulating plasmacytoid dendritic cells." Journal of Immunological Methods 464 (January 2019): 126–30. http://dx.doi.org/10.1016/j.jim.2018.11.001.

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Lim, Su Min, Young-Eun Kim, Won Jun Choi, Ki-Wook Oh, Min-Young Noh, Min-Soo Kwon, Minyeop Nahm, Namshin Kim, Chang-Seok Ki, and Seung Hyun Kim. "CLEC4C p.K210del variant causes impaired cell surface transport in plasmacytoid dendritic cells of amyotrophic lateral sclerosis." Oncotarget 7, no. 18 (March 1, 2016): 24942–49. http://dx.doi.org/10.18632/oncotarget.7886.

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Lim, Suhyeon, Monica Zhang, and Theresa L. Chang. "ACE2-Independent Alternative Receptors for SARS-CoV-2." Viruses 14, no. 11 (November 16, 2022): 2535. http://dx.doi.org/10.3390/v14112535.

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Severe acute respiratory syndrome-related coronavirus (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), is highly contagious and remains a major public health challenge despite the availability of effective vaccines. SARS-CoV-2 enters cells through the binding of its spike receptor-binding domain (RBD) to the human angiotensin-converting enzyme 2 (ACE2) receptor in concert with accessory receptors/molecules that facilitate viral attachment, internalization, and fusion. Although ACE2 plays a critical role in SARS-CoV-2 replication, its expression profiles are not completely associated with infection patterns, immune responses, and clinical manifestations. Additionally, SARS-CoV-2 infects cells that lack ACE2, and the infection is resistant to monoclonal antibodies against spike RBD in vitro, indicating that some human cells possess ACE2-independent alternative receptors, which can mediate SARS-CoV-2 entry. Here, we discuss these alternative receptors and their interactions with SARS-CoV-2 components for ACE2-independent viral entry. These receptors include CD147, AXL, CD209L/L-SIGN/CLEC4M, CD209/DC-SIGN/CLEC4L, CLEC4G/LSECtin, ASGR1/CLEC4H1, LDLRAD3, TMEM30A, and KREMEN1. Most of these receptors are known to be involved in the entry of other viruses and to modulate cellular functions and immune responses. The SARS-CoV-2 omicron variant exhibits altered cell tropism and an associated change in the cell entry pathway, indicating that emerging variants may use alternative receptors to escape the immune pressure against ACE2-dependent viral entry provided by vaccination against RBD. Understanding the role of ACE2-independent alternative receptors in SARS-CoV-2 viral entry and pathogenesis may provide avenues for the prevention of infection by SARS-CoV-2 variants and for the treatment of COVID-19.

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Steinle, Alexander, Veronika Stejfova, Sabrina Kuttruff, Birgit Schittek, and Jessica Spreu. "CLEC2A Is a Novel Skin-Specific, Stimulatory Ligand of Human NK Cells (39.8)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 39.8. http://dx.doi.org/10.4049/jimmunol.182.supp.39.8.

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Abstract The Natural Killer Gene Complex (NKC) encodes for numerous C-type lectin-like receptors (CTLR) variably expressed on lymphocytes and myeloid cells. Well-known representatives of NKC-encoded CTLR are NKG2D, CD69, and Ly49 molecules. However, the NKC also contains a considerable number of genes which are barely characterized. Recently, we described the CLEC2A gene encoding for a new member of the human CLEC2 family of NKC-encoded CTLR. CLEC2A, in contrast to other human CLEC2 family members such as CD69/CLEC2C and AICL/CLEC2B, is virtually not expressed by peripheral leukocytes, but its expression appears restricted to skin. We now report that CLEC2A encodes for a non-disulfide-linked, homodimeric surface CTLR which is expressed on freshly isolated skin cells. Addressing a potential immune-associated function, we find that CLEC2A stimulates cytotoxicity and cytokine release of human NK cells. However, we failed to ascertain CLEC2A engagement by known activating NK receptors. Instead, we identified a hitherto undescribed NKC-encoded CTLR (NKp65) that specifically interacts with CLEC2A and activates NK cytotoxicity. In summary, we define CLEC2A as a skin-specific and NK cell-stimulating CTLR engaging NKp65, a novel activating CTLR which may allow for dedicated immunosurveillance of human skin. This work was supported by funds (SFB 685/A1) of the German Research Foundation (DFG).

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Sharma, Jyotika, Atul Sharma, Anthony Steichen, Christopher Jondle, Brandilyn Binstock, and Bibhuti Mishra. "Antibacterial and pro-resolving mechanisms in lung diseases: role of C-type lectin receptors (INM2P.430)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 56.13. http://dx.doi.org/10.4049/jimmunol.192.supp.56.13.

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Abstract Lower respiratory tract infection with bacteria can lead to sepsis development, a complex immune disorder with systemic hyperinflammation. There are currently no effective therapies for sepsis. To understand the function of specific pulmonary components in regulation of immune responses in this immune disorder, we utilize an acute pulmonary bacterial infection model of Klebsiella pneumoniae (KPn). Nosocomial infections with this opportunistic pathogen account for 5-20% of Gram-negative sepsis cases. C-type lectin receptors (CLRs), expressed mainly by myeloid cells, can shape immune responses in diverse pathological conditions. However, their role in development of pneumonic sepsis is unknown. Our preliminary analysis of a panel of CLRs showed an upregulated expression of two CLRs, Clec4d and Clec4e in the lungs of KPn infected mice. While the wild-type mice were able to resolve a sublethal pneumonic KPn infection, the Clec4d-/- and Clec4e-/- mice displayed increased susceptibility with a progressive increase in bacterial burden, hyperinflammatory response and massive accumulation of neutrophils in lungs. Importantly, we show that coordinated function of Clec4d and Clec4e in neutrophils during bacterial pneumonia, and in a chronic lung disease, leads to control of bacterial growth and hyperinflammation by regulating phagocytosis and efferocytosis (clearance of dead cells). Our studies provide novel insights into regulation of inflammatory derangements in immune disorders.

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Uqdah, Hakim, Shelley Hankins, and Howard J. Eisen. "Something evil this way comes: Proteomic profiling identifies CLEC4C expression as a novel biomarker of primary graft dysfunction after heart transplantation." Journal of Heart and Lung Transplantation 41, no. 3 (March 2022): 269–70. http://dx.doi.org/10.1016/j.healun.2021.12.003.

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Gong, Xiaoting, and Wei Wang. "Profiles of Innate Immune Cell Infiltration and Related Core Genes in Psoriasis." BioMed Research International 2021 (February 23, 2021): 1–8. http://dx.doi.org/10.1155/2021/6656622.

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Psoriasis is an inflammatory skin disease with substantial morbidity. Numerous patients with psoriasis experience recurrence after therapy. The underlying mechanism about psoriasis is still not fully understood. Some evidences suggest that innate immunity may play an unexpected and important role in active severe psoriasis. In this work, the deconvolution algorithm CIBERSORT was conducted to identify the infiltration of innate immune cells and related core genes in psoriatic plaque. Datasets from the Gene Expression Omnibus, including skin samples from 405 psoriasis patients and 91 healthy donors, were downloaded for analysis. Considerable differences of the innate immune cell composition were uncovered between psoriatic plaque and control skin. Results revealed that γδ T cells, resting NK cells, M0 macrophages, M1 macrophages, activated dendritic cells, and neutrophils were significantly increased in psoriatic skin, while resting mast cells and active NK cells were significantly decreased. Moreover, the proportion of M0 macrophages or resting mast cells was found to be associated with disease severity. Spearman correlation analysis suggests that RORC and S100A12 genes were related to disease severity, while genes including S100A12, CLEC4C, IL-19, AIM2, IL-17F, and PPARGC1A were correlated with biologic treatment response. In conclusion, this work displays innate immune status in psoriatic skin and provides novel clues for clinical decisions and mechanism study.

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Ennour-Idrissi, Kaoutar, Dzevka Dragic, Elissar Issa, Annick Michaud, Sue-Ling Chang, Louise Provencher, Francine Durocher, and Caroline Diorio. "DNA Methylation and Breast Cancer Risk: An Epigenome-Wide Study of Normal Breast Tissue and Blood." Cancers 12, no. 11 (October 23, 2020): 3088. http://dx.doi.org/10.3390/cancers12113088.

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Differential DNA methylation is a potential marker of breast cancer risk. Few studies have investigated DNA methylation changes in normal breast tissue and were largely confounded by cancer field effects. To detect methylation changes in normal breast epithelium that are causally associated with breast cancer occurrence, we used a nested case–control study design based on a prospective cohort of patients diagnosed with a primary invasive hormone receptor-positive breast cancer. Twenty patients diagnosed with a contralateral breast cancer (CBC) were matched (1:1) with 20 patients who did not develop a CBC on relevant risk factors. Differentially methylated Cytosine-phosphate-Guanines (CpGs) and regions in normal breast epithelium were identified using an epigenome-wide DNA methylation assay and robust linear regressions. Analyses were replicated in two independent sets of normal breast tissue and blood. We identified 7315 CpGs (FDR < 0.05), 52 passing strict Bonferroni correction (p < 1.22 × 10−7) and 43 mapping to known genes involved in metabolic diseases with significant enrichment (p < 0.01) of pathways involving fatty acids metabolic processes. Four differentially methylated genes were detected in both site-specific and regions analyses (LHX2, TFAP2B, JAKMIP1, SEPT9), and three genes overlapped all three datasets (POM121L2, KCNQ1, CLEC4C). Once validated, the seven differentially methylated genes distinguishing women who developed and who did not develop a sporadic breast cancer could be used to enhance breast cancer risk-stratification, and allow implementation of targeted screening and preventive strategies that would ultimately improve breast cancer prognosis.

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Більше джерел

Дисертації з теми "CLEC4C"

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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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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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/.

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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.

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Smith, Peter. "The status of a presbyter who is no longer a cleric." Theological Research Exchange Network (TREN), 1987. http://www.tren.com.

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Painting-Stubbs, Clare. "Abraham Fleming : writer, cleric and preacher in Elizabethan and Jacobean London." Thesis, Royal Holloway, University of London, 2011. http://repository.royalholloway.ac.uk/items/89fa6719-8bde-2470-3a26-e850544e284e/9/.

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Since his death in 1607, Abraham Fleming has never been completely forgotten about. This thesis covers all aspects of Fleming's life. It begins with his time at Cambridge and the relationships he forged there. It studies his varied and sometimes groundbreaking contributions to the books associated with him (with a focus on his English texts and translations). It also covers his ordination into the Church of England and subsequent career as a chaplain to Charles Howard, earl of Nottingham. It also elucidates his previously unknown life as a curate in the parish of St Nicholas, Deptford and as a deacon and priest St Pancras, Soper Lane, and finally his sermons at Paul's Cross in the grounds of St Paul's Cathedral. Fleming's legacy of at least 52 printed books, which includes original godly protestant treatises, English translations of Latin and Greek classical works, and books commemorating unusual occasions, have ensured that his name lived on in bibliographic catalogues. Since the 1950s a few scholars have considered Fleming's work on Holinshed's Chronicles as significant contributions to the text. However, the subsequent articles that have been written about him have been narrow in scope and at times unreliable. Recent studies of Fleming have considered him only as a minor writer, yet this thesis demonstrates that he was a literary figure of considerable significance. Fleming made an important contribution to the emerging public sphere, as foregrounded by Jurgen Habermas, that was lauded by his contemporaries but he has largely slipped from view. Before this doctoral research little was known about Fleming's career as a preacher in the Church of England, a career in which he proved just as diligent as when he was a “learned corrector” of books. The aim of this thesis has been to throw fresh light on the multi-faceted career of Abraham Fleming and establish him as a leading figure in late-Sixteenth century political and print culture.

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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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Cochin, Christophe. "Marcel Le Clerc (Klerg) et la revue Barr-Heol." Rennes 2, 2005. http://www.theses.fr/2005REN20051.

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Originaire de Plémet, en Haute-Bretagne, l'Abbé Marcel Le Clerc passa sa vie de prêtre dans le Trégor. Militant nationaliste convaincu, il prit fait et cause pour le Mouvement breton. Pendant vingt-cinq ans, il lutta pour maintenir debout sa revue Barr-Heol, née de la rupture avec le Bleun-Brug, essentiellement pour des raisons d'orthographe. Il traduisit également de nombreux livres liturgiques à l'usage des églises catholiques. Il consacra toute sa vie à la défense de la langue bretonne. La période n'était pas propice : entre les années 50 et 80, le breton s'écroulait de toutes parts et il fallait le courage de l'abbé Le Clerc pour maintenir la langue au catéchisme de Buhulien ou dans son bulletin paroissial, " Koulmig ar Gindi ". Il était également passionné par le gallois et la toponymie. Sa mort laissa un vide dans le Mouvement Breton. Mais quelle a été l'influence de l'œuvre de Marcel Le Clerc sur la littérature bretonne aujourd'hui ? Lit-on encore les cent numéros de sa revue vingt-cinq ans après ? Par sa ténacité, sa volonté d'apprendre la langue, d'employer et de diffuser un breton simple et authentique, il restera une figure marquante du renouveau linguistique
Father Marsel Klerg was born in Plemet, in Upper Brittany in 1912. He spent his working life as a priest in Tregor. He was an ardent nationalist and fought all his life for the Breton movement. In 1953, he cut off links with the “Bleun-brug” and managed for 25 years to keep alive his magazine “Barr-Heol” going. He translated many religious books for use in Church. Although he shared a great interest for the Welsh language with his friend Armans ar C'halvez, he spent all his life defending and promoting the Breton language which he began to learn while at school at Saint-Brieuc. This was not an easy task between the years 55 and 80. The use of the language was falling at a catastrophic rate, and Marsel Klerg had to fight to maintain the use of Breton in the catechism of Buhulien or in his parochial bulletin. When he died in 1984, his loss was deeply felt by the Emsav, the Breton movement. 25 years later, it is nearly impossible to find all 100 issues of his magazine. But who nowadays still remembers Father Klerg ? By his courage and his will to learn the language and to use a simple, true and authentic Breton, he will remain an example to all those who knex him, and indeed perhaps for others also

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BIANCHI, ANDREA. "HETERODOXY AND RATIONAL THEOLOGY: JEAN LE CLERC AND ORIGEN." Doctoral thesis, Università Cattolica del Sacro Cuore, 2020. http://hdl.handle.net/10280/73305.

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L’elaborato analizza la ricezione del pensiero di Origene di Alessandria (c. 184-c.253) nell’opera del teologo arminiano Jean Le Clerc (1657-1736), soffermandosi in particolare sulla concezione origeniana della libertà e sulle questioni che vi sono annesse. Tale analisi consente anche di chiarire alcune pratiche argomentative e dinamiche intellettuali, soprattutto riguardanti i dibattiti religiosi ed interconfessionali, nella seconda metà del XVII secolo. L’elaborato è diviso in tre sezioni. La prima, di carattere introduttivo, mira ad indagare le premesse epistemologiche di Le Clerc, nonché la sua relazione con le auctoritates religiose ed intellettuali del passato. La seconda sezione prende in esame le citazioni dirette di Origene presenti nella vasta produzione di Le Clerc, come pure i suoi rimandi all’opera dell’Alessandrino e al suo pensiero, consentendo in questo modo di delineare un quadro preciso dell’Origene letto e reinterpretato da Le Clerc. La terza sezione restringe infine il campo d’indagine allo sguardo che Le Clerc porta sulla dimensione più propriamente teologica di Origene ed in particolar modo su quel nodo di concetti che ruota attorno al tema della libertà umana (peccato originale, grazia e predestinazione, il problema del male). Questo studio mostra come, malgrado l’indubbia, e talvolta malcelata, simpatia per Origene, Le Clerc non possa essere definito tout court un ‘origenista’, dal momento che la sua visione epistemologica, scritturale e teologica lo distanzia da una acritica e piena adesione al pensiero dell’Alessandrino.
The present thesis analyses the reception of the thought of Origen of Alexandria (c. 184-c. 253) in Jean Le Clerc (1657-1736). Its particular focus is on Origen's conception of freedom and the theological doctrines related to it. The goal of this thesis is to uncover, through Le Clerc's use of Origen, some of the argumentative practices and the intellectual dynamics of the time, in particular in religious, especially inter-confessional, debates. This thesis is divided into three main parts. The first part has mainly an introductory character and looks at the epistemological assumptions of Le Clerc and his relationship with intellectual and religious authorities of the past. The second part reviews the various ways in which Le Clerc quoted, referred to or otherwise made use of the thought or the name of Origen in his vast production. This part provides a first result in that it frames, in general, Le Clerc's reception of Origen. This step is, at the same time, also preparatory for the material contained in part three. In the third part, only the material is considered which is strictly related to Origen's idea of freedom and the related theological doctrines of original sin, grace/predestination, and the problem of evil. The result of this analysis, as it appears form the examination of argumentative practices in the previous sections, is that Le Clerc was no simple "Origenist" but neither was he was fully uncommitted to the Origenian cause. A full commitment to Origen, despite this strong sympathy, was still hindered by Le Clerc's epistemological, scriptural and theological outlook.

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BIANCHI, ANDREA. "HETERODOXY AND RATIONAL THEOLOGY: JEAN LE CLERC AND ORIGEN." Doctoral thesis, Università Cattolica del Sacro Cuore, 2020. http://hdl.handle.net/10280/73305.

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Книги з теми "CLEC4C"

Salvatore, R. A. The Cleric Quintet. Renton, WA: TSR, Inc., 1999.

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1947-, Clerc Yves, and Alestchenkoff Catherine, eds. Yves Clerc. Milano: Skira, 2008.

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

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Rioux, Lucien. Julien Clerc. [Paris]: Le Club des stars, 1987.

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Clerc, Alexandre. Alexandre Clerc, ACARCHITECTES. Luzern: Quart Verlag, 2015.

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

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Lemonier, Marc. L' intégrale Julien Clerc: Tout Julien Clerc de A à Z. Grainville: City Éditions, 2007.

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Clerc, Kéké. Kéké Clerc: Erreur judiciaire? Fribourg, Suisse: La Sarine, 1999.

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Laurent, Michèle. Julien Clerc à Bercy. [Paris]: Mengès, 1985.

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1947-, Clerc Julien, ed. Le roman de Julien Clerc. Paris: Le Club des stars, 1988.

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Частини книг з теми "CLEC4C"

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.

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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.

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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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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. "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. "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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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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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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Тези доповідей конференцій з теми "CLEC4C"

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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Riboldi, Elena, Luca Di Tommaso, Nausicaa Clemente, Chiara Raggi, Elisa Forti, Simone Merlin, Fabio Pasqualini, Antonia Follenzi, and Antonio Sica. "Abstract 2677: Role of CLEC4D in inflammation-driven liver carcinogenesis." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2677.

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Yuan, Chang-Zheng. "Hadron Spectroscopy from BES and CLEOc." In HADRON SPECTROSCOPY: Eleventh International Conference on Hadron Spectroscopy. AIP, 2006. http://dx.doi.org/10.1063/1.2176469.

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Plote, S. E. "Optical network architecture choice for Ethernet services - a CLEC's view." In OFCNFOEC 2006. 2006 Optical Fiber Communication Conference and the National Fiber Optic Engineers Conference. IEEE, 2006. http://dx.doi.org/10.1109/ofc.2006.215434.

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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.

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Lu, Hua, and Chris Bailey. "Reliability prediction for IGBT solder joints using Clech Algorithm." In 2016 17th International Conference on Electronic Packaging Technology (ICEPT). IEEE, 2016. http://dx.doi.org/10.1109/icept.2016.7583309.

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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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Hwalek, T., A. Osterburg, M. T. Borchers, and F. X. McCormack. "Role of CLEC5A Signaling Pathway on Pulmonary Osteoclast Differentiation in Silica Challenged Mice." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4048.

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Meddeb, Aref, Abdelwahed Berguiga, and Habib Youssef. "Optimal VPN design: The ILEC/CLEC dilemma." In 2009 IEEE Symposium on Computers and Communications (ISCC). IEEE, 2009. http://dx.doi.org/10.1109/iscc.2009.5202406.

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Zhuang, Xiaodong, Baksho Kaul, Michael Bentley, Zsuzsanna Nagy, Enrico Giraudo, Gavin Bendle, David Gilham, Roy Bicknell, and Steven P. Lee. "Abstract LB-256: Immunotherapy using genetically modified T lymphocytes to target CLEC14A on the tumor vasculature." 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-lb-256.

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