bluuebunny/crossref_metadata_2025_split huggingface dataset:
« Journal de ce qui s’est passé à Versailles depuis l’instant de l’arrivée de Monsieur le comte et de Madame la comtesse du Nord, jusqu’à celui de leur départ »
Authors: Anonyme  
Published: February 2015

La voyage du « comte » et de la « comtesse du Nord » (noms d’emprunt utilisés par le grand-duc Paul de Russie et son épouse Marie Feodorovna) à travers l’Europe en 1781-1782 a fait l’objet d’un nombre considérable d’écrits qui varient aussi bien par leur genre que par le public ciblé. À l’intérieur de ce corpus, le « Journal de ce qui s’est passé à Versailles depuis l’instant de l’arrivée de Monsieur le comte et de Madame la comtesse du Nord, jusqu’à celui de leur départ » (Paris, Archives nationales, O1 824, fos 80ro-90ro) est l’une des principales sources de référence qui permet de retracer l’histoire de l’accueil du couple princier russe à la cour de France entre le 20 mai et le 19 juin 1782. Par sa narration systématique et détaillée des faits, ce document permet de préciser le déroulement chronologique de cette visite « incognito », ses particularités protocolaires, ainsi que le programme culturel et mondain proposé au couple princier. S’ouvrant par la cérémonie de présentation des « illustres voyageurs » au roi de France et à la famille royale, le journal relate toutes les étapes phares de la visite, comme le concert donné dans la Grande Galerie de Versailles, le souper et l’illumination des jardins au Petit Trianon le 6 juin 1782, ou encore le grand bal du 8 juin 1782 dans la salle de spectacles du château. Le « Journal » ne se limite pas aux évènements de parade ; il consigne également des moments de loisirs et des interactions à caractère plus privé : les repas, en particulier avec la famille royale, les promenades dans les jardins versaillais et les visites guidées des collections du roi. En outre, les informations fournies par le texte contribuent à esquisser le réseau de contacts que les voyageurs couronnés russes et les membres de leur entourage établissent à la cour royale de France, ce qui conduit à enrichir notre regard sur les échanges inter-curiaux à l’échelle européenne au xviiie siècle.
Grimm et Once upon a time, entre contes et séries télévisées
Authors: Périer Isabelle 
Published: February 2015

Grimm et Once Upon a Time offrent l’exemple surprenant de deux séries diffusées en même temps et s’appuyant sur un même hypotexte, le conte merveilleux. Et pourtant, ces deux réécritures télévisuelles d’un même substrat intertextuel diffèrent radicalement. L’une s’appuie sur les genres du policier et du fantastique pour se développer de manière plus sérielle que feuilletonnante et se démarque assez vite de l’univers du conte pour développer ses propres intrigues de fantasy urbaine. L’autre reste plus fidèle à l’intertexte merveilleux mais elle l’agence de manière à créer un vaste monde transfictionnel et métadiscursif tourné vers le thème de la famille, dans un emprunt au soap opera. Ainsi, les réécritures contemporaines et télévisuelles du conte merveilleux visent-elles davantage à « faire monde » qu’à réellement rendre hommage à leur lointain ancêtre littéraire.
La merveille dans la peau : le tatouage féerique ou le nouveau pays imaginaire
Authors: Chassagnol Anne 
Published: February 2015

Il s’agit d’explorer ici un phénomène sociétal émergent qui se répand de manière virale outre-Manche alors qu’il est, à ce jour, relativement peu étudié par les spécialistes du genre. Le tatouage littéraire déplace le territoire du merveilleux, hors de son vecteur livresque traditionnel, sous une forme autre que celle du modèle cinématographique, vidéo ou numérique, en imaginant un nouvel espace qui permet d’inscrire le merveilleux à même la peau. Le tatouage littéraire n’est pas un phénomène récent en tant que tel ; la nouveauté est plutôt à chercher du côté de la nature des textes tatoués qui semblent provenir de plus en plus fréquemment du corpus de la littérature de jeunesse. Le succès des romans de J. K. Rowling n’est sans doute pas étranger à cette mode, si l’on en juge par le nombre de sites consacrés aux tatouages inspirés de la série Harry Potter. Le tatouage littéraire merveilleux peut se manifester sous forme de citation, célèbre ou cryptique, référencée ou pas. Quels sont donc les textes de littérature de jeunesse les plus communément tatoués ? S’agit-il de textes récents ? Que peut-on en conclure sur le renouveau de la culture de jeunesse contemporaine ?
Avatars des Centaures : du mythe à la fantasy
Authors: Gallé Hélène 
Published: February 2015

La figure du centaure, constamment réactualisée au fil des siècles, connaît surtout une véritable diffusion à une date très récente, dans la littérature destinée à la jeunesse et plus généralement dans la fantasy qui touche un public plus large. Y a-t-il permanence ou évolution de la figure mythique du centaure ? Comment le centaure s’intègre-t-il dans le nouveau pays des merveilles qui s’élabore dans la littérature contemporaine ?
Egress of Mature Murine Regulatory T Cells from the Thymus Requires RelA
Authors: Fukazawa Taro , Hiraiwa Noriko , Umemura Takeshi , Mise-Omata Setsuko , Obata Yuichi , Doi Takahiro 
Published: February 2015

Abstract
The mechanism of egress of mature regulatory T cells (Tregs) from the thymus to the periphery remains enigmatic, as does the nature of those factors expressed in the thymic environment. In this study, we examined the fate of thymic Tregs in TNF-α/RelA double-knockout (TA-KO) mice, because TA-KO mice retain a Treg population in the thymus but have only a small Treg population at the periphery. Transplantation of whole TA-KO thymus to under the kidney capsule of Rag1-null mice failed to induce the production of donor-derived splenic Tregs expressing neuropilin-1, which is reported to be a marker of naturally occurring Tregs, indicating that TA-KO thymic Tregs either do not leave the thymus or are lost at the periphery. We next transplanted enriched TA-KO thymic Tregs to the peripheries of TA-KO mice and traced mouse survival. Transplantation of TA-KO thymic Tregs rescued the lethality in TA-KO mice, demonstrating that TA-KO thymic Tregs remained functional at the periphery. The TA-KO thymic Treg population had highly demethylated CpG motifs in the foxp3 locus, indicating that the cells were arrested at a late mature stage. Also, the population included a large subpopulation of Tregs expressing IL-7Rα, which is a possible marker of late-stage mature Tregs. Finally, TA-KO fetal liver chimeric mice developed a neuropilin-1+ splenic Treg population from TA-KO cells, suggesting that Treg arrest was caused by a lack of RelA in the thymic environment. Taken together, these results suggest that egress of mature Tregs from the thymus depends on RelA in the thymic environment.
c-FLIP Protects T Lymphocytes from Apoptosis in the Intrinsic Pathway
Authors: He Ming-Xiao , He You-Wen 
Published: February 2015

Abstract
Apoptosis can be induced by either death receptors on the plasma membrane (extrinsic pathway) or the damage of the genome and/or cellular organelles (intrinsic pathway). Previous studies suggest that cellular caspase 8 (FLICE)-like inhibitory protein (c-FLIP) promotes cell survival in death receptor–induced apoptosis pathway in T lymphocytes. Independent of death receptor signaling, mitochondria sense apoptotic stimuli and mediate the activation of effector caspases. Whether c-FLIP regulates mitochondrion-dependent apoptotic signals remains unknown. In this study, c-FLIP gene was deleted in mature T lymphocytes in vitro, and the role of c-FLIP protein in intrinsic apoptosis pathway was studied. In resting T cells treated with the intrinsic apoptosis inducer, c-FLIP suppressed cytochrome c release from mitochondria. Bim-deletion rescued the enhanced apoptosis in c-FLIP–deficient T cells, whereas inhibition of caspase 8 did not. Different from activated T cells, there was no necroptosis or increase in reactive oxygen species in c-FLIP–deficient resting T cells. These data suggest that c-FLIP is a negative regulator of intrinsic apoptosis pathway in T lymphocytes.
Proinflammatory Responses and Higher IL-10 Production by T Cells Correlate with Protection against Malaria during Pregnancy and Delivery Outcomes
Authors: Requena Pilar , Barrios Diana , Robinson Leanne J. , Samol Paula , Umbers Alexandra J. , Wangnapi Regina , Ome-Kaius Maria , Rosanas-Urgell Anna , Mayor Alfredo , López Marta , de Lazzari Elisa , Arévalo-Herrera Myriam , Fernández-Becerra Carmen , del Portillo Hernando , Chitnis Chetan E. , Siba Peter M. , Rogerson Stephen , Mueller Ivo , Bardají Azucena , Menéndez Clara , Dobaño Carlota 
Published: February 2015

Abstract
Pregnancy triggers immunological changes aimed to tolerate the fetus. However, it has not been properly addressed whether similar changes occur in tropical areas with high infection pressure and whether these changes render women more susceptible to infectious diseases. We compared the frequencies of T cell subsets, including regulatory T cells, in pregnant and nonpregnant women from Papua New Guinea, a high malaria transmission area, and from Spain, a malaria-free country. We also assessed the relationship among these cellular subsets, malaria infection, and delivery outcomes. CD4+FOXP3+CD127low T cells (Tregs) were decreased in pregnant women in both countries but were not associated with malaria infection or poor delivery outcomes. An expansion of IFN-γ–producing cells and intracytoplasmic IFN-γ levels was found in pregnant compared with nonpregnant women only in Papua New Guinea. Increased CD4+IL-10+IFN-γ+ frequencies and Treg–IFN-γ production were found in women with current Plasmodium falciparum infection. Higher CD4+IL-10−IFN-γ+ T cells frequencies and production of proinflammatory cytokines (including TNF and IL-2) at recruitment (first antenatal visit) had a protective association with birth weight and future (delivery) P. falciparum infection, respectively. Higher intracellular IL-10 levels in T cells had a protective association with future P. falciparum infection and hemoglobin levels at delivery. The protective associations were found also with nonmalaria-specific T cell responses. Treg frequencies positively correlated with plasma eotaxin concentrations, but this subset did not express eotaxin receptor CCR3. Thus, an activated immune system during pregnancy might contribute to protection against malaria during pregnancy and poor delivery outcomes.
Inhibiting STAT5 by the BET Bromodomain Inhibitor JQ1 Disrupts Human Dendritic Cell Maturation
Authors: Toniolo Patricia A. , Liu Suhu , Yeh Jennifer E. , Moraes-Vieira Pedro M. , Walker Sarah R. , Vafaizadeh Vida , Barbuto José Alexandre M. , Frank David A. 
Published: February 2015

Abstract
Maturation of dendritic cells (DCs) is required to induce T cell immunity, whereas immature DCs can induce immune tolerance. Although the transcription factor STAT5 is suggested to participate in DC maturation, its role in this process remains unclear. In this study, we investigated the effect of STAT5 inhibition on LPS-induced maturation of human monocyte-derived DCs (Mo-DCs). We inhibited STAT5 by treating Mo-DCs with JQ1, a selective inhibitor of BET epigenetic readers, which can suppress STAT5 function. We found that JQ1 inhibits LPS-induced STAT5 phosphorylation and nuclear accumulation, thereby attenuating its transcriptional activity in Mo-DCs. The diminished STAT5 activity results in impaired maturation of Mo-DCs, as indicated by defective upregulation of costimulatory molecules and CD83, as well as reduced secretion of IL-12p70. Expression of constitutively activated STAT5 in JQ1-treated Mo-DCs overcomes the effects of JQ1 and enhances the expression of CD86, CD83, and IL-12. The activation of STAT5 in Mo-DCs is mediated by GM-CSF produced following LPS stimulation. Activated STAT5 then leads to increased expression of both GM-CSF and GM-CSFR, triggering an autocrine loop that further enhances STAT5 signaling and enabling Mo-DCs to acquire a more mature phenotype. JQ1 decreases the ability of Mo-DCs to induce allogeneic CD4+ and CD8+ T cell proliferation and production of proinflammatory cytokines. Furthermore, JQ1 leads to a reduced generation of inflammatory CD8+ T cells and decreased Th1 differentiation. Thus, JQ1 impairs LPS-induced Mo-DC maturation by inhibiting STAT5 activity, thereby generating cells that can only weakly stimulate an adaptive-immune response. Therefore, JQ1 could have beneficial effects in treating T cell–mediated inflammatory diseases.
Properdin Provides Protection from Citrobacter rodentium–Induced Intestinal Inflammation in a C5a/IL-6–Dependent Manner
Authors: Jain Umang , Cao Qi , Thomas Nikhil A. , Woodruff Trent M. , Schwaeble Wilhelm J. , Stover Cordula M. , Stadnyk Andrew W. 
Published: February 2015

Abstract
Citrobacter rodentium is an attaching and effacing mouse pathogen that models enteropathogenic and enterohemorrhagic Escherichia coli in humans. The complement system is an important innate defense mechanism; however, only scant information is available about the role of complement proteins during enteric infections. In this study, we examined the impact of the lack of properdin, a positive regulator of complement, in C. rodentium–induced colitis. Following infection, properdin knockout (PKO) mice had increased diarrhea and exacerbated inflammation combined with defective epithelial cell–derived IL-6 and greater numbers of colonizing bacteria. The defect in the mucosal response was reversed by administering exogenous properdin to PKO mice. Then, using in vitro and in vivo approaches, we show that the mechanism behind the exacerbated inflammation of PKO mice is due to a failure to increase local C5a levels. We show that C5a directly stimulates IL-6 production from colonic epithelial cells and that inhibiting C5a in infected wild-type mice resulted in defective epithelial IL-6 production and exacerbated inflammation. These outcomes position properdin early in the response to an infectious challenge in the colon, leading to complement activation and C5a, which in turn provides protection through IL-6 expression by the epithelium. Our results unveil a previously unappreciated mechanism of intestinal homeostasis involving complement, C5a, and IL-6 during bacteria-triggered epithelial injury.
The NLRP1 Inflammasome Attenuates Colitis and Colitis-Associated Tumorigenesis
Authors: Williams Tere M. , Leeth Rachel A. , Rothschild Daniel E. , Coutermarsh-Ott Sheryl L. , McDaniel Dylan K. , Simmons Alysha E. , Heid Bettina , Cecere Thomas E. , Allen Irving C. 
Published: February 2015

Abstract
Nucleotide-binding domain and leucine-rich repeat (NLR) proteins are a diverse family of pattern recognition receptors that are essential mediators of inflammation and host defense in the gastrointestinal system. Recent studies have identified a subgroup of inflammasome forming NLRs that modulate the mucosal immune response during inflammatory bowel disease (IBD) and colitis associated tumorigenesis. To better elucidate the contribution of NLR family members in IBD and cancer, we conducted a retrospective analysis of gene expression metadata from human patients. These data revealed that NLRP1, an inflammasome forming NLR, was significantly dysregulated in IBD and colon cancer. To better characterize the function of NLRP1 in disease pathogenesis, we used Nlrp1b−/− mice in colitis and colitis-associated cancer models. In this paper, we report that NLRP1 attenuates gastrointestinal inflammation and tumorigenesis. Nlrp1b−/− mice demonstrated significant increases in morbidity, inflammation, and tumorigenesis compared with wild-type animals. Similar to data previously reported for related inflammsome forming NLRs, the increased inflammation and tumor burden was correlated with attenuated levels of IL-1β and IL-18. Further mechanistic studies using bone marrow reconstitution experiments revealed that the increased disease pathogenesis in the Nlrp1b−/− mice was associated with nonhematopoietic-derived cells and suggests that NLRP1 functions in the colon epithelial cell compartment to attenuate tumorigenesis. Taken together, these data identify NLRP1 as an essential mediator of the host immune response during IBD and cancer. These findings are consistent with a model whereby multiple NLR inflammasomes attenuate disease pathobiology through modulating IL-1β and IL-18 levels in the colon.
IL-1 Receptor Type 2 Suppresses Collagen-Induced Arthritis by Inhibiting IL-1 Signal on Macrophages
Authors: Shimizu Kenji , Nakajima Akiko , Sudo Katsuko , Liu Yang , Mizoroki Atsuhiko , Ikarashi Tetsuro , Horai Reiko , Kakuta Shigeru , Watanabe Toshiki , Iwakura Yoichiro 
Published: February 2015

AbstractIL-1α and IL-1β (in this article referred to as IL-1) play important roles in host defense against infection and inflammatory diseases. IL-1R1 is the receptor for IL-1, and IL-1R2 is suggested to be a decoy receptor, because it lacks the signal-transducing TIR domain in the cytoplasmic part. However, the roles of IL-1R2 in health and disease remain largely unknown. In this study, we generated EGFP-knock-in Il1r2−/− mice and showed that they were highly susceptible to collagen-induced arthritis, an animal model for rheumatoid arthritis in which the expression of IL-1R2 is augmented in inflammatory joints. Il1r2 was highly expressed in neutrophils but had only low expression in other cells, including monocytes and macrophages. Ab production and T cell responses against type II collagen were normal in Il1r2−/− mice. Despite the high expression in neutrophils, no effects of Il1r2 deficiency were observed; however, we found that production of inflammatory mediators in response to IL-1 was greatly enhanced in Il1r2−/− macrophages. These results suggest that IL-1R2 is an important regulator of arthritis by acting specifically on macrophages as a decoy receptor for IL-1.
Biased Agonism as a Novel Strategy To Harness the Proresolving Properties of Melanocortin Receptors without Eliciting Melanogenic Effects
Authors: Montero-Melendez Trinidad , Gobbetti Thomas , Cooray Sadani N. , Jonassen Thomas E. N. , Perretti Mauro 
Published: February 2015

AbstractThere is a need for novel approaches to control pathologies with overexuberant inflammatory reactions. Targeting melanocortin (MC) receptors represents a promising therapy for obesity and chronic inflammation, but lack of selectivity and safety concerns limit development. A new way to increase selectivity of biological effects entails the identification of biased agonists. In this study, we characterize the small molecule AP1189 as a biased agonist at receptors MC1 and MC3. Although not provoking canonical cAMP generation, AP1189 addition to MC1 or MC3, but not empty vector, transfected HEK293 cells caused ERK1/2 phosphorylation, a signaling responsible for the proefferocytic effect evoked in mouse primary macrophages. Added to macrophage cultures, AP1189 reduced cytokine release, an effect reliant on both MC1 and MC3 as evident from the use of Mc1r−/− and Mc3r−/− macrophages. No melanogenesis was induced by AP1189 in B16-F10 melanocytes. In vivo, oral AP1189 elicited anti-inflammatory actions in peritonitis and, upon administration at the peak of inflammation, accelerated the resolution phase by ∼3-fold. Finally, given the clinical efficacy of adrenocorticotropin in joint diseases, AP1189 was tested in experimental inflammatory arthritis, where this biased agonist afforded significant reduction of macroscopic and histological parameters of joint disruption. These proof-of-concept analyses with AP1189, an active oral anti-inflammatory and resolution-promoting compound, indicate that biased agonism at MC receptors is an innovative, viable approach to yield novel anti-inflammatory molecules endowed with a more favorable safety profile.
Collagen Induces Maturation of Human Monocyte-Derived Dendritic Cells by Signaling through Osteoclast-Associated Receptor
Authors: Schultz Heidi S. , Nitze Louise M. , Zeuthen Louise H. , Keller Pernille , Gruhler Albrecht , Pass Jesper , Chen Jianhe , Guo Li , Fleetwood Andrew J. , Hamilton John A. , Berchtold Martin W. , Panina Svetlana 
Published: February 2015

Abstract
Osteoclast-associated receptor (OSCAR) is widely expressed on human myeloid cells. Collagen types (Col)I, II, and III have been described as OSCAR ligands, and ColII peptides can induce costimulatory signaling in receptor activator for NF-κB–dependent osteoclastogenesis. In this study, we isolated collagen as an OSCAR-interacting protein from the membranes of murine osteoblasts. We have investigated a functional outcome of the OSCAR–collagen interaction in human monocyte-derived dendritic cells (DCs). OSCAR engagement by ColI/II-induced activation/maturation of DCs is characterized by upregulation of cell surface markers and secretion of cytokines. These collagen-matured DCs (Col-DCs) were efficient drivers of allogeneic and autologous naive T cell proliferation. The T cells expanded by Col-DCs secreted cytokines with no clear T cell polarization pattern. Global RNA profiling revealed that multiple proinflammatory mediators, including cytokines and cytokine receptors, components of the stable immune synapse (namely CD40, CD86, CD80, and ICAM-1), as well as components of TNF and TLR signaling, are transcriptional targets of OSCAR in DCs. Our findings indicate the existence of a novel pathway by which extracellular matrix proteins locally drive maturation of DCs during inflammatory conditions, for example, within synovial tissue of rheumatoid arthritis patients, where collagens become exposed during tissue remodeling and are thus accessible for interaction with infiltrating precursors of DCs.
Functional Analysis of a Complement Polymorphism (rs17611) Associated with Rheumatoid Arthritis
Authors: Giles Joanna L. , Choy Ernest , van den Berg Carmen , Morgan B. Paul , Harris Claire L. 
Published: February 2015

Abstract
Complement is implicated in the pathogenesis of rheumatoid arthritis (RA); elevated levels of complement activation products have been measured in plasma, synovial fluid, and synovial tissues of patients. Complement polymorphisms are associated with RA in genome-wide association studies. Coding-region polymorphisms may directly impact protein activity; indeed, we have shown that complement polymorphisms affecting a single amino acid change cause subtle changes in individual component function that in combination have dramatic effects on complement activity and disease risk. In this study, we explore the functional consequences of a single nucleotide polymorphism (SNP) (rs17611) encoding a V802I polymorphism in C5 and propose a mechanism for its link to RA pathology. Plasma levels of C5, C5a, and terminal complement complex were measured in healthy and RA donors and correlated to rs17611 polymorphic status. Impact of the SNP on C5 functionality was assessed. Plasma C5a levels were significantly increased and C5 levels significantly lower with higher copy number of the RA risk allele for rs17611, suggesting increased turnover of C5 V802. Functional assays using purified C5 variants revealed no significant differences in lytic activity, suggesting that increased C5 V802 turnover was not mediated by complement convertase enzymes. C5 is also cleaved in vivo by proteases; the C5 V802 variant was more sensitive to cleavage with elastase and the “C5a” generated was biologically active. We hypothesize that this SNP in C5 alters the rate at which elastase generates active C5a in rheumatoid joints, hence recruiting neutrophils to the site thus maintaining a state of inflammation in arthritic joints.