bluuebunny/crossref_metadata_2025_split huggingface dataset:
Éloge des liaisons techniques
Authors: Rabot Jean-Martin 
Published: May 2011

Résumé Du point de vue d’une sociologie du quotidien et de l’imaginaire, les nouvelles technologies ne peuvent pas être envisagées comme source d’aliénation ou d’homogénéisation. Elles ne conduisent pas à l’annihilation du discours ontologique (Freund) ou des potentialités imaginatives de l’homme (Ellul). Ni même à « l’arraisonnement » de l’être (Heidegger), dans le but de mobiliser l’homme comme simple objet technique. Les nouvelles technologies sont avant tout vecteurs de socialité. De surcroît, dans la postmodernité, le développement technologique est parfaitement compatible avec le réinvestissement mythologique (Durand) et le retour aux valeurs communautaires (Maffesoli). Les liaisons techniques qui se développent au sein des réseaux informatiques sont avant tout productrices de relations et d’interactions sociales.
Médiations technologiques dans l'espace urbain contemporain
Authors: Leite Julieta 
Published: May 2011

Résumé La diffusion de l’usage des technologies de l’information et de la communication dans notre environnement quotidien est à l’origine d’une nouvelle configuration spatiale et d’une mutation des formes relationnelles qui en sont indissociables. Ces changements mettent également en œuvre une pensée partagée axée sur les représentations collectives dans le quotidien en reconnaissant la primauté de l’affect, au sens d’« être affecté » par les objets technologiques, l’espace et son expérience. La réflexion est ainsi fondée sur la médiation numérique dans ces trois dimensions de l’espace urbain (physique, sociale et imaginaire), où nous observons une hybridation des interactions socio-spatiales avec l’information et la communication numériques.
L'esthétique de l'écoute
Authors: Oliveira Madalena 
Published: May 2011

Résumé La radio est profondément liée à la vie quotidienne à une époque où la communication de masse s’est étendue à la densité sensitive du son et à la force significative de messages sonores qui cherchent l’immédiateté comme élément distinctif. « Médium chaud » dans l’expression de McLuhan, la radio correspond non seulement à une technique sophistiquée de transmission directe d’information, mais aussi et surtout à un art dont le langage a autant de rationalité que d’émotivité. Essayant de produire des portraits de la réalité sans images, la radio est porteuse par le son en général et par la parole en particulier du pouvoir constitutif de l’actualité. D’ailleurs, en concentrant toute sa vivacité imaginative dans un seul sens, le discours radiophonique essaye d’être séduisant et attractif. En effet, c’est de la nature même de la radio d’être émotive, passionnée, poignante. Voilà pourquoi elle est liée à l’imaginaire de plusieurs générations, non seulement en ce qui concerne la diffusion de l’information, mais aussi dans la mesure où elle se rapporte à une expérience esthétique particulière.
De comment est (re)fait l'espace-entre : A Cidade dos Objectos [La Ville des Objets] (Augusto Alves da Silva)
Authors: Pires Helena 
Published: May 2011

Résumé L’exercice sémiotique que nous proposons dans ce contexte repose sur une conception ontologique et épistémologique de l’espace qui, dans une certaine mesure, se rapproche de la notion d’espace parcouru de Michel de Certeau. L’auteur s’intéresse aux « énonciations pédestres », aux pratiques de l’espace qui sont étrangères à une grammaire universalisante. Cette dimension de l’espace étant celle que nous chercherons à aborder, l’objectif de cet essai est de centrer notre attention sur les objets qui s’interposent sur les trajets sémiotiques en énonciation. Nous considérons que ces mêmes trajets sont composés de réseaux de relations hétérogènes, incorporés par des acteurs humains et non humains. Les contributions de Latour, de Donna Haraway et de Deleuze et de Guattari, entre autres, sont fondamentales pour une élucidation réflexive sur la nature de ces relations. L’espace s’ouvrant à la possibilité de la coexistence, nous chercherons à relater la coexistence matérielle des différents corps, des différents acteurs, des manières particulières selon lesquelles les objets transbordent de sens inusités et se transforment en éléments créatifs qui produisent indéfiniment l’espace, en même temps qu’ils sont produits par lui et partagent sa nature ineffable.
Plis et fragments
Authors: Gonçalves Albertino 
Published: May 2011

Résumé Ce texte se propose un exercice fort simple : déceler quelques figures typiques du baroque dans les annonces publicitaires récentes destinées à la télévision et au cinéma. Écrire sur l’audio-visuel comporte toujours un risque à ne pas ignorer : le risque d’écrire des séries de légendes sans images 1 .
Self-Tolerance Checkpoints in CD4 T Cells Specific for a Peptide Derived from the B Cell Antigen Receptor
Authors: Detanico Thiago , Heiser Ryan A. , Aviszus Katja , Bonorino Cristina , Wysocki Lawrence J. 
Published: May 2011

AbstractLinked recognition of Ag by B and T lymphocytes is ensured in part by a state of tolerance acquired by CD4 T cells to germline-encoded sequences within the B cell Ag receptor (BCR). We sought to determine how such tolerance is attained when a peptide from the BCR variable (V) region is expressed by small numbers of B cells as it is in the physiological state. Mixed bone marrow (BM) chimeras were generated using donor BM from mice with B cells that expressed a transgene (Tg)-encoded κ L chain and BM from TCR Tg mice in which the CD4 T cells (CA30) were specific for a Vκ peptide encoded by the κTg. In chimeras where few B cells express the κTg, many CA30 cells were deleted in the thymus. However, a substantial fraction survived to the CD4 single-positive stage. Among single-positive CA30 thymocytes, few reached maturity and migrated to the periphery. Maturation was strongly associated with, and likely promoted by, expression of an endogenous TCR α-chain. CD4+ CA30 cells that reached peripheral lymphoid tissues were Ag-experienced and anergic, and some developed into regulatory cells. These findings reveal several checkpoints and mechanisms that enforce a state of self-tolerance in developing T cells specific for BCR V region sequences, thus ensuring that T cell help to B cells occurs through linked recognition of foreign Ag.
Aborted Germinal Center Reactions and B Cell Memory by Follicular T Cells Specific for a B Cell Receptor V Region Peptide
Authors: Heiser Ryan A. , Snyder Christopher M. , St. Clair James , Wysocki Lawrence J. 
Published: May 2011

Abstract
A fundamental problem in immunoregulation is how CD4+ T cells react to immunogenic peptides derived from the V region of the BCR that are created by somatic mechanisms, presented in MHC II, and amplified to abundance by B cell clonal expansion during immunity. BCR neo Ags open a potentially dangerous avenue of T cell help in violation of the principle of linked Ag recognition. To analyze this issue, we developed a murine adoptive transfer model using paired donor B cells and CD4 T cells specific for a BCR-derived peptide. BCR peptide-specific T cells aborted ongoing germinal center reactions and impeded the secondary immune response. Instead, they induced the B cells to differentiate into short-lived extrafollicular plasmablasts that secreted modest quantities of Ig. These results uncover an immunoregulatory process that restricts the memory pathway to B cells that communicate with CD4 T cells via exogenous foreign Ag.
Forced Expression of HLA-DM at the Surface of Dendritic Cells Increases Loading of Synthetic Peptides on MHC Class II Molecules and Modulates T Cell Responses
Authors: Pezeshki Abdul Mohammad , Côté Marie-Hélène , Azar Georges A. , Routy Jean-Pierre , Boulassel Mohamed-Rachid , Thibodeau Jacques 
Published: May 2011

Abstract
Adoptive transfer of autologous dendritic cells (DCs) loaded with tumor-associated CD4 and CD8 T cell epitopes represents a promising avenue for the immunotherapy of cancer. In an effort to increase the loading of therapeutic synthetic peptides on MHC II molecules, we used a mutant of HLA-DM (DMY) devoid of its lysosomal sorting motif and that accumulates at the cell surface. Transfection of DMY into HLA-DR+ cells resulted in increased loading of the exogenously supplied HA307–318 peptide, as well as increased stimulation of HA-specific T cells. Also, on transduction in mouse and human DCs, DMY increased loading of HEL48–61 and of the tumor Ag-derived gp100174–190 peptides, respectively. Interestingly, expression of DMY at the surface of APCs favored Th1 differentiation over Th2. Finally, we found that DMY− and DMY+ mouse APCs differentially stimulated T cell hybridomas sensitive to the fine conformation of peptide–MHC II complexes. Taken together, our results suggest that the overexpression of HLA-DMY at the plasma membrane of DCs may improve quantitatively, but also qualitatively, the presentation of CD4 T cell epitopes in cellular vaccine therapies for cancer.
High-Affinity IgE Receptors on Dendritic Cells Exacerbate Th2-Dependent Inflammation
Authors: Sallmann Eva , Reininger Bärbel , Brandt Sabine , Duschek Nikolaus , Hoflehner Elisabeth , Garner-Spitzer Erika , Platzer Barbara , Dehlink Eleonora , Hammer Martina , Holcmann Martin , Oettgen Hans C. , Wiedermann Ursula , Sibilia Maria , Fiebiger Edda , Rot Antal , Maurer Dieter 
Published: May 2011

Abstract
The IgE-mediated and Th2-dependent late-phase reaction remains a mechanistically enigmatic and daunting element of human allergic inflammation. In this study, we uncover the FcεRI on dendritic cells (DCs) as a key in vivo component of this form of allergy. Because rodent, unlike human, DCs lack FcεRI, this mechanism could be revealed only by using a new transgenic mouse model with human-like FcεRI expression on DCs. In the presence of IgE and allergen, FcεRI+ DCs instructed naive T cells to differentiate into Th2 cells in vitro and boosted allergen-specific Th2 responses and Th2-dependent eosinophilia at the site of allergen exposure in vivo. Thus, FcεRI on DCs drives the cascade of pathogenic reactions linking the initial allergen capture by IgE with subsequent Th2-dominated T cell responses and the development of late-phase allergic tissue inflammation.
Group X Secretory Phospholipase A2 Enhances TLR4 Signaling in Macrophages
Authors: Shridas Preetha , Bailey William M. , Talbott Kayla R. , Oslund Rob C. , Gelb Michael H. , Webb Nancy R. 
Published: May 2011

Abstract
Secretory phospholipase A2s (sPLA2) hydrolyze glycerophospholipids to liberate lysophospholipids and free fatty acids. Although group X (GX) sPLA2 is recognized as the most potent mammalian sPLA2 in vitro, its precise physiological function(s) remains unclear. We recently reported that GX sPLA2 suppresses activation of the liver X receptor in macrophages, resulting in reduced expression of liver X receptor-responsive genes including ATP-binding cassette transporters A1 (ABCA1) and G1 (ABCG1), and a consequent decrease in cellular cholesterol efflux and increase in cellular cholesterol content (Shridas et al. 2010. Arterioscler. Thromb. Vasc. Biol. 30: 2014–2021). In this study, we provide evidence that GX sPLA2 modulates macrophage inflammatory responses by altering cellular cholesterol homeostasis. Transgenic expression or exogenous addition of GX sPLA2 resulted in a significantly higher induction of TNF-α, IL-6, and cyclooxygenase-2 in J774 macrophage-like cells in response to LPS. This effect required GX sPLA2 catalytic activity, and was abolished in macrophages that lack either TLR4 or MyD88. The hypersensitivity to LPS in cells overexpressing GX sPLA2 was reversed when cellular free cholesterol was normalized using cyclodextrin. Consistent with results from gain-of-function studies, peritoneal macrophages from GX sPLA2-deficient mice exhibited a significantly dampened response to LPS. Plasma concentrations of inflammatory cytokines were significantly lower in GX sPLA2-deficient mice compared with wild-type mice after LPS administration. Thus, GX sPLA2 amplifies signaling through TLR4 by a mechanism that is dependent on its catalytic activity. Our data indicate this effect is mediated through alterations in plasma membrane free cholesterol and lipid raft content.
MUC5AC Expression through Bidirectional Communication of Notch and Epidermal Growth Factor Receptor Pathways
Authors: Kang Jin Hyun , Lee Eun Hee , Park Sung Woo , Chung Il Yup 
Published: May 2011

Abstract
Hyperproduction of goblet cells and mucin in the airway epithelium is an important feature of airway inflammatory diseases. We investigated the involvement of Notch signaling in MUC5AC expression in NCI-H292 cells, a human lung carcinoma cell line. Epidermal growth factor (EGF) stimulated generation of the Notch intracellular domain (NICD) in a RBP-Jκ–dependent manner. Treatment with γ-secretase inhibitors L-685,458 or DAPT or introduction of small interfering RNA directed against Notch1 reduced EGF-induced MUC5AC expression. The inhibitory effect of L-685,458 on EGF-induced MUC5AC mRNA and protein expression was also observed in primary human bronchial epithelial cells. Blockage of Notch signaling with L-685,458 or Notch siRNA resulted in a decrease in EGF-induced phosphorylation of ERK. These results suggested that ERK activation is necessary for the regulation of EGF receptor (EGFR)–mediated MUC5AC expression by Notch signaling. Conversely, forced expression of NICD induced both EGFR and ERK phosphorylation with MUC5AC expression even in the absence of EGF. Treatment of the NICD-expressing cells with EGF further augmented ERK phosphorylation in an additive manner. The ERK phosphorylation induced by exogenous NICD was inhibited by treatment with an Ab that antagonizes EGFR activity as well as by inhibitors of EGFR and ERK, implying that Notch signaling induces MUC5AC expression by activating the EGFR pathway. Collectively, these results suggest that MUC5AC expression is regulated by a bidirectional circuit between Notch and EGFR signaling pathways.
Reduction of the Peripheral Blood CD56bright NK Lymphocyte Subset in FTY720-Treated Multiple Sclerosis Patients
Authors: Johnson Trina A. , Evans Barbara L. , Durafourt Bryce A. , Blain Manon , Lapierre Yves , Bar-Or Amit , Antel Jack P. 
Published: May 2011

Abstract
FTY720 (fingolimod) treatment of multiple sclerosis (MS) results in lymphopenia due to increased recruitment into and decreased egress from secondary lymphoid organs of CCR7+ lymphocytes. Although absolute numbers of NK lymphocytes were reported as being unaltered in FTY720-treated MS patients (MS-FTY), such analyses did not detect a change in a minor subset. Because expression of CCR7 has been described on CD56bright NK cells, a minority population of NK cells, we investigated the effect of FTY720 treatment on the phenotype and function of human NK cells in the peripheral circulation of MS patients. MS-FTY patients displayed a decreased proportion of peripheral CD56brightCD62L+CCR7+ NK cells compared with untreated MS and healthy donors. In vitro treatment with FTY720-P increased migration of untreated donor NK cells to CXCL12 while reducing the response to CX3CL1 with similar migration responses seen in NK cells from MS-FTY patients. FTY720-P inhibited sphingosine 1-phosphate–directed migration of CD56bright and CD56dim NK cells subsets from untreated healthy donors. IL-12– and IL-15–stimulated NK cells from MS-FTY patients displayed similar capacity to produce IFN-γ, TNF, IL-10, and MIP-1α cytokines/chemokines compared with NK cells from untreated healthy donors and displayed comparable levels of degranulation in response to K562 tumor cells compared with untreated donors. Subset alterations and function of NK cell populations will need to be considered as part of assessing overall immunosurveillance capacity of patients with MS who will receive sustained FTY720 therapy.
Rescue of Tumor-Infiltrating Lymphocytes from Activation-Induced Cell Death Enhances the Antitumor CTL Response in CD5-Deficient Mice
Authors: Tabbekh Mouna , Franciszkiewicz Katarzyna , Haouas Houda , Lécluse Yann , Benihoud Karim , Raman Chander , Mami-Chouaib Fathia 
Published: May 2011

Abstract
The CD5 coreceptor is expressed on all T cells and on the B1a B cell subset. It is associated with TCR and BCR, and modulates intracellular signals initiated by both Ag receptor complexes. Human CD5 contributes to regulation of the antitumor immune response and susceptibility of specific CTL to activation-induced cell death (AICD) triggered by the tumor. In this study, we compared the T cell response to the B16F10 melanoma engrafted into CD5-deficient and wild-type C57BL/6 mice. Compared with wild-type mice, CD5 knockout animals displayed delayed tumor growth, associated with tumor infiltration by T cell populations exhibiting a more activated phenotype and enhanced antitumor effector functions. However, control of tumor progression in CD5−/− mice was transient due to increased AICD of CD8+ tumor-infiltrating T lymphocytes. Remarkably, in vivo protection of T cells from TCR-mediated apoptosis by an adenovirus engineered to produce soluble Fas resulted in a dramatic reduction in tumor growth. Our data suggest that recruitment of tumor-specific T cells in the tumor microenvironment occurs at early stages of cancer development and that tumor-mediated AICD of tumor-infiltrating T lymphocytes is most likely involved in tumor escape from the immune system.
A Role for IL-27 in Limiting T Regulatory Cell Populations
Authors: Tait Wojno Elia D. , Hosken Nancy , Stumhofer Jason S. , O’Hara Aisling C. , Mauldin Elizabeth , Fang Qun , Turka Laurence A. , Levin Steven D. , Hunter Christopher A. 
Published: May 2011

Abstract
IL-27 is a cytokine that regulates Th function during autoimmune and pathogen-induced immune responses. Although previous studies have shown that regulatory T cells (Tregs) express the IL-27R, and that IL-27 inhibits forkhead box P3 upregulation in vitro, little is known about how IL-27 influences Tregs in vivo. The studies presented in this article show that mice that overexpress IL-27 had decreased Treg frequencies and developed spontaneous inflammation. Although IL-27 did not cause mature Tregs to downregulate forkhead box P3, transgenic overexpression in vivo limited the size of a differentiating Treg population in a bone marrow chimera model, which correlated with reduced production of IL-2, a vital cytokine for Treg maintenance. These data identify an indirect role for IL-27 in shaping the Treg pool.
A Balance of Bruton’s Tyrosine Kinase and SHIP Activation Regulates B Cell Receptor Cluster Formation by Controlling Actin Remodeling
Authors: Liu Chaohong , Miller Heather , Hui King Lam , Grooman Brian , Bolland Silvia , Upadhyaya Arpita , Song Wenxia 
Published: May 2011

Abstract
The activation of the BCR, which initiates B cell activation, is triggered by Ag-induced self-aggregation and clustering of receptors at the cell surface. Although Ag-induced actin reorganization is known to be involved in BCR clustering in response to membrane-associated Ag, the underlying mechanism that links actin reorganization to BCR activation remains unknown. In this study, we show that both the stimulatory Bruton’s tyrosine kinase (Btk) and the inhibitory SHIP-1 are required for efficient BCR self-aggregation. In Btk-deficient B cells, the magnitude of BCR aggregation into clusters and B cell spreading in response to an Ag-tethered lipid bilayer is drastically reduced, compared with BCR aggregation observed in wild-type B cells. In SHIP-1−/− B cells, although surface BCRs aggregate into microclusters, the centripetal movement and growth of BCR clusters are inhibited, and B cell spreading is increased. The persistent BCR microclusters in SHIP-1−/− B cells exhibit higher levels of signaling than merged BCR clusters. In contrast to the inhibition of actin remodeling in Btk-deficient B cells, actin polymerization, F-actin accumulation, and Wiskott–Aldrich symptom protein phosphorylation are enhanced in SHIP-1−/− B cells in a Btk-dependent manner. Thus, a balance between positive and negative signaling regulates the spatiotemporal organization of the BCR at the cell surface by controlling actin remodeling, which potentially regulates the signal transduction of the BCR. This study suggests a novel feedback loop between BCR signaling and the actin cytoskeleton.
Mechanical Interactions between Dendritic Cells and T Cells Correlate with T Cell Responsiveness
Authors: Lim Tong Seng , Mortellaro Alessandra , Lim Chwee Teck , Hämmerling Günter J. , Ricciardi-Castagnoli Paola 
Published: May 2011

Abstract
Ag recognition is achieved through the communication across intercellular contacts between T cells and APCs such as dendritic cells (DC). Despite remarkable progress in delineating detailed molecular components at the intercellular contacts, little is known about the functional roles of physical cross-junctional adhesion between T and DC in shaping T cell responses. In addition, the mechanisms underlying sensitivity and specificity of Ag discrimination by T cells at intercellular contacts remain to be elucidated. In this study, we use single-cell force spectroscopy to probe the mechanical interactions between DC and T cells in response to stimulation with a panel of altered peptide ligands. The results show that intercellular interactions of DC–T cell conjugates exhibited different ranges of interaction forces in peptide-dependent manners that match the ability of the peptides to activate T cells. Elevated calcium mobilization and IL-2 secretion by T cells were only promoted in response to antigenic peptides that induce strong interaction forces, suggesting that mechanically stable DC–T cell contacts are crucial for driving T cell activation. Strong interactions were not solely dependent on cell-surface molecules such as TCRs and the adhesion molecule LFA-1, but were also controlled by cytoskeletal dynamics and the integrity of membrane lipid rafts. These data provide novel mechanical insights into the effect of Ag affinity on intercellular contacts that align with T cell responsiveness.
IL-13 Antibodies Influence IL-13 Clearance in Humans by Modulating Scavenger Activity of IL-13Rα2
Authors: Kasaian Marion T. , Raible Donald , Marquette Kimberly , Cook Timothy A. , Zhou Simon , Tan Xiang-Yang , Tchistiakova Lioudmila 
Published: May 2011

Abstract
Human studies using Abs to two different, nonoverlapping epitopes of IL-13 suggested that epitope specificity can have a clinically significant impact on clearance of IL-13. We propose that Ab modulation of IL-13 interaction with IL-13Rα2 underlies this effect. Two Abs were administered to healthy subjects and mild asthmatics in separate dose-ranging studies and allergen-challenge studies. IMA-638 allows IL-13 interaction with IL-13Rα1 or IL-13Rα2 but blocks recruitment of IL-4Rα to the IL-13/IL-13Rα1 complex, whereas IMA-026 competes with IL-13 interaction with IL-13Rα1 and IL-13Rα2. We found ∼10-fold higher circulating titer of captured IL-13 in subjects treated with IMA-026 compared with those administered IMA-638. To understand how this difference could be related to epitope, we asked whether either Ab affects IL-13 internalization through cell surface IL-13Rα2. Humans inducibly express cell surface IL-13Rα2 but lack the soluble form that regulates IL-13 responses in mice. Cells with high IL-13Rα2 expression rapidly and efficiently depleted extracellular IL-13, and this activity persisted in the presence of IMA-638 but not IMA-026. The potency and efficiency of this clearance pathway suggest that cell surface IL-13Rα2 acts as a scavenger for IL-13. These findings could have important implications for the design and characterization of IL-13 antagonists.