bluuebunny/crossref_metadata_2025_split huggingface dataset:
Une passion de l'égalité particulièrement insatiable en France
Authors: Forsé Michel 
Published: March 2014

Pour les opinions de la population d’une majorité de pays dans le monde, les inégalités salariales sont en hausse et contribuent à former une société injuste, tandis que dans le même temps la mondialisation accroît les écarts entre les pays riches et les pays pauvres. Cette perception des inégalités et de leur évolution n’est pas nécessairement en adéquation avec les niveaux ou les mouvements de ces inégalités tels que révélés par les indices statistiques usuels appliqués nationalement. Ainsi, en France, on juge davantage qu’ailleurs que les inégalités de revenus sont trop grandes, bien qu’elles se situent dans la moyenne des pays suivis par l’OCDE. Et là où elles sont élevées, comme aux États-Unis, on les trouve peu importantes. La France se caractérise au total par une « passion de l’égalité » très prégnante qui s’explique par le décalage entre un idéal égalitaire de justice sociale (commun à tous les pays) et cette perception d’inégalités plus fortes qu’ailleurs.
De la monnaie cosmopolitique
Authors: Parodi Maxime 
Published: March 2014

Une monnaie cosmopolitique est une monnaie unique à plusieurs nations et fondée explicitement sur une forme de co-souveraineté. Une telle monnaie n’est possible qu’en acceptant une politique monétaire et des politiques budgétaires et fiscales fondées sur des raisons partagées, où chacun est responsable des engagements monétaires qu’il prend et coresponsable de la capacité de chacun à mener une politique économique adéquate. Pour durer, cette monnaie exige une attention soutenue sur les divergences macroéconomiques entre les partenaires et les difficultés que rencontre chacun ; elle impose une concertation ouverte sur les raisons de ces divergences et de ces difficultés ; elle nécessite une force de propositions sur les remèdes possibles, à court, moyen et long terme ; enfin, elle exige la coopération volontaire de chacun, à condition toutefois d’en avoir la capacité. Une telle coopération monétaire repose sur une union cosmopolitique, qui est comme une société toujours en train de se faire mais jamais achevée entre des partenaires conservant leur souveraineté. Une telle union n’écrit pas de contrat social ; elle ne promulgue pas nécessairement de lois ou de traités pour résoudre ses problèmes, même lorsqu’elle est convaincue de la nécessité d’une réponse collective au problème. Face à certains problèmes hautement conflictuels, il n’y aura ainsi pas d’autre choix que d’en passer par le jugement commun des gouvernements cosouverains. Dans ce cas, la seule garantie que peuvent espérer obtenir les partenaires de l’union, c’est que le jugement commun traduira le mieux possible l’esprit de l’union, la volonté de continuer à faire le chemin ensemble.
Du double affrontement ontologique/axiologique autour de la résilience aux risques de catastrophe : les spécificités de l’approche française
Authors: Quenault Béatrice 
Published: March 2014

L’engouement croissant autour de la résilience dans les sociétés urbanisées peut s’interpréter comme le signe d’une impuissance assumée face à un certain nombre de risques, climatiques notamment, dont la réduction serait désormais jugée inaccessible. Toutefois, derrière la quête implicite de la « catastrophe acceptable » que sous-tend la mise en avant du concept de résilience se profile une double occasion d’affrontement, « ontologique » (à caractère épistémologique) entre deux visions opposées de la résilience, et « axiologique » (de nature politique) entre deux approches de la gestion des risques en vue de prévenir les catastrophes. Face à ce constat, cet article s’attache au travers des spécificités de l’approche française des politiques publiques en matière de gestion des risques de catastrophe d’origine climatique en milieu urbain à souligner l’opposition entre, d’une part, la vision dominante focalisée sur la résilience réactive de court terme, et, d’autre part, celle systémique plus marginalement répandue mettant l’accent sur la résilience proactive de long terme. Alors que la première participe d’une simple instrumentalisation de la résilience dans la gestion des risques et la planification urbaine en continuité avec le « business as usual » pour rendre acceptable ce qui a priori ne l’est pas, la seconde participe au contraire d’une revendication de rénovation politique profonde destinée à rendre effective la transition soutenable des systèmes urbains.
Tissue Requirements for Establishing Long-Term CD4+ T Cell–Mediated Immunity following Leishmania donovani Infection
Authors: Bunn Patrick T. , Stanley Amanda C. , de Labastida Rivera Fabian , Mulherin Alexander , Sheel Meru , Alexander Clare E. , Faleiro Rebecca J. , Amante Fiona H. , Montes De Oca Marcela , Best Shannon E. , James Kylie R. , Kaye Paul M. , Haque Ashraful , Engwerda Christian R. 
Published: March 2014

Abstract
Organ-specific immunity is a feature of many infectious diseases, including visceral leishmaniasis caused by Leishmania donovani. Experimental visceral leishmaniasis in genetically susceptible mice is characterized by an acute, resolving infection in the liver and chronic infection in the spleen. CD4+ T cell responses are critical for the establishment and maintenance of hepatic immunity in this disease model, but their role in chronically infected spleens remains unclear. In this study, we show that dendritic cells are critical for CD4+ T cell activation and expansion in all tissue sites examined. We found that FTY720-mediated blockade of T cell trafficking early in infection prevented Ag-specific CD4+ T cells from appearing in lymph nodes, but not the spleen and liver, suggesting that early CD4+ T cell priming does not occur in liver-draining lymph nodes. Extended treatment with FTY720 over the first month of infection increased parasite burdens, although this associated with blockade of lymphocyte egress from secondary lymphoid tissue, as well as with more generalized splenic lymphopenia. Importantly, we demonstrate that CD4+ T cells are required for the establishment and maintenance of antiparasitic immunity in the liver, as well as for immune surveillance and suppression of parasite outgrowth in chronically infected spleens. Finally, although early CD4+ T cell priming appeared to occur most effectively in the spleen, we unexpectedly revealed that protective CD4+ T cell–mediated hepatic immunity could be generated in the complete absence of all secondary lymphoid tissues.
Distinct Requirements for Activation of NKT and NK Cells during Viral Infection
Authors: Tyznik Aaron J. , Verma Shilpi , Wang Qiao , Kronenberg Mitchell , Benedict Chris A. 
Published: March 2014

Abstract
NK cells are key regulators of innate defense against mouse CMV (MCMV). Like NK cells, NKT cells also produce high levels of IFN-γ rapidly after MCMV infection. However, whether similar mechanisms govern activation of these two cell types, as well as the significance of NKT cells for host resistance, remain unknown. In this article, we show that, although both NKT and NK cells are activated via cytokines, their particular cytokine requirements differ significantly in vitro and in vivo. IL-12 is required for NKT cell activation in vitro but is not sufficient, whereas NK cells have the capacity to be activated more promiscuously in response to individual cytokines from innate cells. In line with these results, GM-CSF–derived dendritic cells activated only NK cells upon MCMV infection, consistent with their virtual lack of IL-12 production, whereas Flt3 ligand–derived dendritic cells produced IL-12 and activated both NK and NKT cells. In vivo, NKT cell activation was abolished in IL-12−/− mice infected with MCMV, whereas NK cells were still activated. In turn, splenic NK cell activation was more IL-18 dependent. The differential requirements for IL-12 and IL-18 correlated with the levels of cytokine receptor expression by NK and NKT cells. Finally, mice lacking NKT cells showed reduced control of MCMV, and depleting NK cells further enhanced viral replication. Taken together, our results show that NKT and NK cells have differing requirements for cytokine-mediated activation, and both can contribute nonredundantly to MCMV defense, revealing that these two innate lymphocyte subsets function together to fine-tune antiviral responses.
IL-13 Orchestrates Resolution of Chronic Intestinal Inflammation via Phosphorylation of Glycogen Synthase Kinase-3β
Authors: Fichtner-Feigl Stefan , Kesselring Rebecca , Martin Maria , Obermeier Florian , Ruemmele Petra , Kitani Atsushi , Brunner Stefan M. , Haimerl Michael , Geissler Edward K. , Strober Warren , Schlitt Hans J. 
Published: March 2014

Abstract
Spontaneous amelioration of inflammation (often accompanied by fibrosis) is a well-known, but poorly understood, outcome of many chronic inflammatory processes. We studied this phenomenon in a chronic trinitrobenzene sulfonic acid–induced colitis model, an experimental colitis in mice that we showed to ultimately undergo spontaneous resolution, despite continued trinitrobenzene sulfonic acid stimulation. Analysis of the mechanism of this resolution revealed that it was critically dependent on IL-13 activation of STAT6, followed by phosphorylation (inactivation) of glycogen synthase kinase-3β, at least in part via STAT6 induction of p38 MAPK. Such glycogen synthase kinase-3β inactivation causes changes in CREB and p65 DNA-binding activity that favors decreased proinflammatory IL-17 production and increased anti-inflammatory IL-10 production. Thus, in this case, IL-13 acts as a molecular switch that leads to resolution of inflammation.
Innate PI3K p110δ Regulates Th1/Th17 Development and Microbiota-Dependent Colitis
Authors: Steinbach Erin C. , Kobayashi Taku , Russo Steven M. , Sheikh Shehzad Z. , Gipson Gregory R. , Kennedy Samantha T. , Uno Jennifer K. , Mishima Yoshiyuki , Borst Luke B. , Liu Bo , Herfarth Hans , Ting Jenny P. Y. , Sartor R. Balfour , Plevy Scott E. 
Published: March 2014

Abstract
The p110δ subunit of class IA PI3K modulates signaling in innate immune cells. We previously demonstrated that mice harboring a kinase-dead p110δ subunit (p110δKD) develop spontaneous colitis. Macrophages contributed to the Th1/Th17 cytokine bias in p110δKD mice through increased IL-12 and IL-23 expression. In this study, we show that the enteric microbiota is required for colitis development in germfree p110δKD mice. Colonic tissue and macrophages from p110δKD mice produce significantly less IL-10 compared with wild-type mice. p110δKD APCs cocultured with naive CD4+ Ag-specific T cells also produce significantly less IL-10 and induce more IFN-γ– and IL-17A–producing CD4+ T cells compared with wild-type APCs. Illustrating the importance of APC–T cell interactions in colitis pathogenesis in vivo, Rag1−/−/p110δKD mice develop mild colonic inflammation and produced more colonic IL-12p40 compared with Rag1−/− mice. However, CD4+CD45RBhigh/low T cell Rag1−/−/p110δKD recipient mice develop severe colitis with increased percentages of IFN-γ– and IL-17A–producing lamina propria CD3+CD4+ T cells compared with Rag1−/− recipient mice. Intestinal tissue samples from patients with Crohn’s disease reveal significantly lower expression of PIK3CD compared with intestinal samples from non–inflammatory bowel disease control subjects (p &lt; 0.05). PIK3CD expression inversely correlates with the ratio of IL12B:IL10 expression. In conclusion, the PI3K subunit p110δ controls homeostatic APC–T cell interactions by altering the balance between IL-10 and IL-12/23. Defects in p110δ expression and/or function may underlie the pathogenesis of human inflammatory bowel disease and lead to new therapeutic strategies.
MAPK Phosphotase 5 Deficiency Contributes to Protection against Blood-Stage Plasmodium yoelii 17XL Infection in Mice
Authors: Cheng Qianqian , Zhang Qingfeng , Xu Xindong , Yin Lan , Sun Lin , Lin Xin , Dong Chen , Pan Weiqing 
Published: March 2014

Abstract
Cell-mediated immunity plays a crucial role in the development of host resistance to asexual blood-stage malaria infection. However, little is known of the regulatory factors involved in this process. In this study, we investigated the impact of MAPK phosphotase 5 (MKP5) on protective immunity against a lethal Plasmodium yoelii 17XL blood-stage infection using MKP5 knockout C57BL/6 mice. Compared with wild-type control mice, MKP5 knockout mice developed significantly lower parasite burdens with prolonged survival times. We found that this phenomenon correlated with a rapid and strong IFN-γ–dependent cellular immune response during the acute phase of infection. Inactivation of IFN-γ by the administration of a neutralizing Ab significantly reduced the protective effects in MKP5 knockout mice. By analyzing IFN-γ production in innate and adaptive lymphocyte subsets, we observed that MKP5 deficiency specifically enhanced the IFN-γ response mediated by CD4+ T cells, which was attributable to the increased stimulatory capacity of splenic CD11c+ dendritic cells. Furthermore, following vaccination with whole blood-stage soluble plasmodial Ag, MKP5 knockout mice acquired strongly enhanced Ag-specific immune responses and a higher level of protection against subsequent P. yoelii 17XL challenge. Finally, we found the enhanced response mediated by MKP5 deficiency resulted in a lethal consequence in mice when infected with nonlethal P. yoelii 17XNL. Thus, our data indicate that MKP5 is a potential regulator of immune resistance against Plasmodium infection in mice, and that an understanding of the role of MKP5 in manipulating anti-malaria immunity may provide valuable information on the development of better control strategies for human malaria.
Gene Expression in the Gitr Locus Is Regulated by NF-κB and Foxp3 through an Enhancer
Authors: Tone Yukiko , Kidani Yoko , Ogawa Chihiro , Yamamoto Kouhei , Tsuda Masato , Peter Christian , Waldmann Herman , Tone Masahide 
Published: March 2014

Abstract
Glucocorticoid-induced TNFR (Gitr) and Ox40, two members of the TNFR superfamily, play important roles in regulating activities of effector and regulatory T cells (Treg). Their gene expression is induced by T cell activation and further upregulated in Foxp3+ Treg. Although the role of Foxp3 as a transcriptional repressor in Treg is well established, the mechanisms underlying Foxp3-mediated transcriptional upregulation remain poorly understood. This transcription factor seems to upregulate expression not only of Gitr and Ox40, but also other genes, including Ctla4, Il35, Cd25, all critical to Treg function. To investigate how Foxp3 achieves such upregulation, we analyzed its activity on Gitr and Ox40 genes located within a 15.1-kb region. We identified an enhancer located downstream of the Gitr gene, and both Gitr and Ox40 promoter activities were shown to be upregulated by the NF-κB–mediated enhancer activity. We also show, using the Gitr promoter, that the enhancer activity was further upregulated in conjunction with Foxp3. Foxp3 appears to stabilize NF-κB p50 binding by anchoring it to the enhancer, thereby enabling local accumulation of transcriptional complexes containing other members of the NF-κB and IκB families. These findings may explain how Foxp3 can activate expression of certain genes while suppressing others.
IFN-γ or IFN-α Ameliorates Chronic Proliferative Dermatitis by Inducing Expression of Linear Ubiquitin Chain Assembly Complex
Authors: Tamiya Hironari , Terao Mika , Takiuchi Tsuyoshi , Nakahara Masaki , Sasaki Yoshiteru , Katayama Ichiro , Yoshikawa Hideki , Iwai Kazuhiro 
Published: March 2014

Abstract
The linear ubiquitin chain assembly complex (LUBAC) ubiquitin ligase complex, composed of HOIL-1L–interacting protein (HOIP), heme-oxidized IRP2 ubiquitin ligase-1L (HOIL-1L), and SHANK-associated RH domain protein, specifically generates linear polyubiquitin chains and is involved in NF-κB activation. Lack of SHANK-associated RH domain protein, which drastically reduces the amount of HOIP and HOIL-1L, causes chronic proliferative dermatitis (cpdm) in mice. Impaired NF-κB activation and augmented apoptosis have been implicated in the pathogenesis of cpdm in mice. In this study, we found that IFN-γ increased the amount of LUBAC by inducing HOIP and HOIL-1L mRNA transcription and enhanced the signal-induced NF-κB activation in embryonic fibroblasts, keratinocytes, and bone marrow–derived macrophages from wild-type and/or cpdm mice; however, IFN-γ failed to augment NF-κB activation in mouse embryonic fibroblasts lacking linear polyubiquitination activity of LUBAC. Moreover, s.c. injection of IFN-γ for 3 wk into the skin of cpdm mice increased the amount of HOIP, suppressed apoptosis, and ameliorated the dermatitis. Inhibition of keratinocyte apoptosis by IFN-γ injection suppressed neutrophil, macrophage, and mast cell infiltration and the amount of TNF-α in the skin of cpdm mice. Similarly, IFN-α also enhanced the amount of HOIP as well as NF-κB activation, inhibited apoptosis, and ameliorated cpdm dermatitis. These results indicate that the IFNs enhance NF-κB activation and ameliorate cpdm dermatitis by augmenting expression of HOIP and HOIL-1L and linear polyubiquitination activity of LUBAC.
Functional NK Cell Repertoires Are Maintained through IL-2Rα and Fas Ligand
Authors: Felices Martin , Lenvik Todd R. , Ankarlo Dave E. M. , Foley Bree , Curtsinger Julie , Luo Xianghua , Blazar Bruce R. , Anderson Stephen K. , Miller Jeffrey S. 
Published: March 2014

Abstract
Acquisition of a functional NK cell repertoire, known as education or licensing, is a complex process mediated through inhibitory receptors that recognize self. We found that NK cells containing self-killer Ig-like receptors for cognate HLA ligand in vivo were less susceptible to apoptosis. In vitro IL-15 withdrawal showed that uneducated NK cells upregulated Bim and Fas. Conversely, educated NK cells upregulated Fas ligand (FasL) under these conditions. Induction of cell death and Bim expression on uneducated cells correlated with increased IL-2Rα expression. Overexpression and knockdown studies showed that higher IL-2Rα limits NK cell survival in a novel manner that is independent from the role of IL-2 in activation-induced cell death. To study the role of FasL in induction of IL-2Rαhi NK cell death, a coculture assay with FasL-blocking Abs was used. IL-15 withdrawal led to FasL-dependent killing of IL-2Rαhi NK cells by more educated IL-2Rαlo NK cells. Finally, CMV reactivation induces a potent long-lasting population of licensed NK cells with enhanced survival. These findings show that education-dependent NK cell survival advantages and killing of uneducated NK cells result in the maintenance of a functional repertoire, which may be manipulated to exploit NK cells for cancer immunotherapy.
B Cell Differentiation Is Associated with Reprogramming the CCCTC Binding Factor–Dependent Chromatin Architecture of the Murine MHC Class II Locus
Authors: Majumder Parimal , Scharer Christopher D. , Choi Nancy M. , Boss Jeremy M. 
Published: March 2014

Abstract
The transcriptional insulator CCCTC binding factor (CTCF) was shown previously to be critical for human MHC class II (MHC-II) gene expression. Whether the mechanisms used by CTCF in humans were similar to that of the mouse and whether the three-dimensional chromatin architecture created was specific to B cells were not defined. Genome-wide CTCF occupancy was defined for murine B cells and LPS-derived plasmablasts by chromatin immunoprecipitation sequencing. Fifteen CTCF sites within the murine MHC-II locus were associated with high CTCF binding in B cells. Only one-third of these sites displayed significant CTCF occupancy in plasmablasts. CTCF was required for maximal MHC-II gene expression in mouse B cells. In B cells, a subset of the CTCF regions interacted with each other, creating a three-dimensional architecture for the locus. Additional interactions occurred between MHC-II promoters and the CTCF sites. In contrast, a novel configuration occurred in plasma cells, which do not express MHC-II genes. Ectopic CIITA expression in plasma cells to induce MHC-II expression resulted in high levels of MHC-II proteins, but did not alter the plasma cell architecture completely. These data suggest that reorganizing the three-dimensional chromatin architecture is an epigenetic mechanism that accompanies the silencing of MHC-II genes as part of the cell fate commitment of plasma cells.
Hysteresis and coercivity of hematite
Authors: Özdemir Özden , Dunlop David J. 
Published: March 2014

AbstractIn room‐temperature hysteresis, 14 submicron hematites (0.12‐0.45 µm) had large coercive forces Hc (150‐350 mT), while 22 natural 1‐5.5 mm hematite crystals had Hc = 0.8‐23 mT (basal‐plane measurements). Single‐domain (SD) and multidomain (MD) hematites owe their high Hc mainly to magnetoelastic anisotropy, caused in fine particles by internal strains and in large crystals by defects like dislocations, with a smaller contribution by triaxial magnetocrystalline anisotropy. A strong correlation between Hc and the defect moment Md measured below hematite's Morin transition also favors magnetoelastic control. Saturation remanence/saturation magnetization ratios Mrs/Ms and coercivity ratios Hcr/Hc (Hcr is remanent coercive force) are distinctive: Mrs/Ms = 0.5‐0.9, Hcr/Hc = 1.02‐1.17 for MD hematites; Mrs/Ms = 0.5‐0.7, Hcr/Hc = 1.45‐1.62 for SD hematites. In high‐temperature (20‐690°C) hysteresis, Hc(T) ~ Ms(T) to a power 1.8‐2.4 above 385°C. Magnetoelastic wall pinning by crystal defects is thus more likely than control by domain nucleation which depends on magnetocrystalline anisotropy. Our results compare well with existing Hc vs. crystal size d data. A suggested peak in Hc around 15 µm and a proposed slope change around 100 µm are both questionable. Using only near‐saturation data, Hc varies continuously as d−0.61 from ≈0.1 µm to 2 mm. The SD threshold size d0 may be >15 µm but there is no strong evidence that d0 ≈100 µm. Direct domain observations are needed to settle the question. Augmented data sets for Hc and Mrs vs. d show that SD hematite is increasingly affected by thermal fluctuations below ≈0.3 µm and generally confirm a superparamagnetic threshold size ds of 0.025‐0.03 µm.
Hedgehog Signalling
Authors: Cruz‐Migoni Sara Betania , Borycki Anne‐Gaëlle 
Published: March 2014

AbstractHedgehog (Hh) proteins are a family of secreted factors with morphogen activities that have essential role during embryonic development and in adulthood. Mechanisms underlying the production and reception, as well as the signal transduction pathway of Hh proteins, are highly conserved between invertebrates and vertebrates. However, despite this evolutionary conservation, a major divergence is the pathway's association with primary cilia in vertebrates. Hh proteins act both as short‐range and long‐range factors in the control of cell fate specification and cell differentiation, cell proliferation, tissue patterning and morphogenesis during embryonic development. Hh proteins are also involved in tumour formation. Knowledge of this pathway has been instrumental in recent therapeutic approaches aiming at downregulating Hh signalling in cancers.Key Concepts:Hedgehog signalling is conserved during evolution.Hedgehog is a morphogen, specifying distinct cell types at different concentrations.Hedgehog acts as a short‐ and long‐range signalling molecule.Hedgehog has essential role in cell fate specification and differentiation and in cell proliferation and survival.Hedgehog signalling is implicated in cancer.