bluuebunny/crossref_metadata_2025_split huggingface dataset:
Du déracinement à la commercialisation de la nostalgie du Sud par les race records
Authors: Djavadzadeh Keivan 
Published: January 2015

Cet article porte sur la commercialisation de la nostalgie du Sud par les enregistrements de blues féminin des années 1920 (race records). Au tournant du siècle, un important mouvement de migration voit de nombreux Africains-Américains du Sud rural (en majorité des hommes) rejoindre le Nord urbain que la bourgeoisie noire présente comme un nouveau Jourdain. Le déclenchement de la Première Guerre mondiale accentue le phénomène : le flux d’immigrés européens cesse et les industriels du Nord n’ont d’autre choix que de démarcher et d’embaucher des Noirs du Sud dans leurs usines. Les espoirs sont néanmoins vite déçus et une crise identitaire frappe les migrants, stigmatisés car jugés inadaptés à la vie urbaine. Dans le même temps des femmes noires vont enregistrer le blues, entretenir la nostalgie du Sud et transmettre le souvenir de la migration. Si l’intégration des Noirs au modèle fordiste permit l’émergence d’un marché noir et la commercialisation du blues, j’affirme que c’est un besoin identitaire qui a rendu nécessaire le développement des race records : contre le désespoir qu’aurait pu inspirer le déracinement, les migrants tirèrent un parti créatif de la nostalgie qui les aida à survivre dans un monde hostile.
L’évocation mémorielle des boîtes à chansons au Québec
Authors: Trottier Danick 
Published: January 2015

Cette étude porte sur le projet québécois La mémoire des boîtes à chansons, qui a vu le jour en 1996 sous forme d’émissions télévisuelles à la chaîne Canal D, pour ensuite se matérialiser en un coffret de deux disques avec témoignages à l’appui dans le livret. La nostalgie qui se joue dans la mémoire évoquée repose à la fois sur les thèmes des chansons et le rappel du lieu où normalement elles ont vu le jour, soit les boîtes à chansons des années 1960. Comme lieu de mémoire, le coffret montre la façon dont la canonisation du mouvement des chansonniers peut mettre à profit un sentiment de nostalgie de manière à consolider une appartenance générationnelle chez les baby-boomers, d’où les interactions à l’œuvre entre canon et nostalgie. Dans ce contexte, une certaine industrie de la musique pop québécoise, soit celle généralement associée à l’héritage de Guy Latraverse, propose un objet de consommation gouverné par un devoir de mémoire.
« Le train qui siffle ». Nostalgie et modernité dans la chanson country-western au Québec
Authors: Lefrançois Catherine 
Published: January 2015

La chanson country-western, qui fait son apparition au Québec en 1942 avec les chansons de guerre de Roland Lebrun, a toujours exploité la nostalgie. Il s’agit d’un èthos fermement ancré dans ce répertoire et il est signalé, dans les enregistrements du country-western émergent des années 1940 et 1950, par plusieurs marqueurs sonores qui font notamment appel à un usage particulier du second mode de phonation et de la réverbération. Il s’agit alors d’une nostalgie typique de la modernité populaire, axée sur les souvenirs personnels et les récits individuels. Ce premier country-western s’inscrit par ailleurs dans la modernité de plusieurs manières, notamment par son succès médiatique. Cette modernité semble aujourd’hui complètement occultée et si la nostalgie demeure un élément clé de la chanson country-western, celle-ci est devenue une nostalgie plus traditionnelle et conservatrice, orientée vers une idéalisation du passé.
Nonapoptotic and Extracellular Activity of Granzyme B Mediates Resistance to Regulatory T Cell (Treg) Suppression by HLA-DR−CD25hiCD127lo Tregs in Multiple Sclerosis and in Response to IL-6
Authors: Bhela Siddheshvar , Kempsell Christine , Manohar Monali , Dominguez-Villar Margarita , Griffin Russell , Bhatt Pooja , Kivisakk-Webb Pia , Fuhlbrigge Robert , Kupper Thomas , Weiner Howard , Baecher-Allan Clare 
Published: January 2015

Abstract
In autoimmune patients, regulatory T cells (Tregs) are increasingly found to be unable to suppress patient-derived T cells, an outcome referred to as Treg resistance. In this study, we show that CD4 T cells from patients with multiple sclerosis resist suppression by patient-derived or healthy donor–derived ex vivo Tregs. Importantly, we report that granzyme B (GzmB) contributes to this Treg resistance via a novel, apoptosis-independent mechanism. We show that memory CD4+CD127loFOXP3+ Treg subsets do not express GzmB, whereas activated, nonregulatory CD4 T cells isolated from patients with multiple sclerosis express higher levels of GzmB than do cells from healthy donors. In contrast to the intracellular GzmB that mediates apoptosis, GzmB can be found in extracellular fluids where it is hypothesized to regulate other cellular processes. In this study, we show that providing extracellular GzmB strongly inhibits Treg suppression, without altering Treg viability. However, when GzmB and GzmB-specific inhibitor are both provided to the cocultures, Treg suppression occurs. Thus, these data suggest that a novel activity of extracellular GzmB is to regulate Treg suppression. Additionally, we find that the suppression-abrogating cytokine IL-6 augments GzmB expression by human CD4 T cells, and it inhibits Treg suppression via this nonapoptotic GzmB-mediated mechanism. Lastly, in examining the mechanism whereby GzmB inhibits Treg function, we show that extracellular GzmB reduces Treg expression of CD39 and programmed death ligand 1. Collectively, these data indicate that extracellular GzmB plays an unexpected, nonapoptotic role in regulating Treg suppression and suggest that inactivation of specifically the extracellular activity of GzmB may be an efficacious therapeutic in autoimmunity.
MHC Class II Presentation Is Controlled by the Lysosomal Small GTPase, Arl8b
Authors: Michelet Xavier , Garg Salil , Wolf Benjamin J. , Tuli Amit , Ricciardi-Castagnoli Paola , Brenner Michael B. 
Published: January 2015

Abstract
Dendritic cells (DCs) are specialized APCs with the ability to prime naive T cells. DCs first sample Ags from the environment and then orchestrate their processing and loading onto MHC class II (MHC II) Ag-presenting molecules in lysosomes. Once MHC II molecules have bound a peptide, the MHC II–peptide complex is delivered to the cell surface for presentation to CD4+ T cells. Regulation of Ag uptake via macropinocytosis and phagocytosis has been extensively studied, as well as trafficking in early endocytic vesicles notably regulated by the small GTPase Rab5 and its effectors. However, little is known about the regulators of Ag delivery from early endosomes to lysosomal compartments where the proper pH, proteases, MHC II, invariant chain, and HLA-DM reside, awaiting exogenous Ags for loading. In this article, we report the crucial role of the small GTPase ADP-ribosylation factor-like 8b (Arl8b) in MHC II presentation in DCs. We show for the first time, to our knowledge, that Arl8b localizes to MHC II compartments in DCs and regulates formation of MHC II–peptide complexes. Arl8b-silenced DCs display a defect in MHC II–Ag complex formation and its delivery to the cell surface during infection resulting in a defect in T cell recognition. Our results highlight the role of Arl8b as a trafficking regulator of the late stage of complex formation and MHC II presentation in DCs.
CD28 Inhibits T Cell Adhesion by Recruiting CAPRI to the Plasma Membrane
Authors: Strazza Marianne , Azoulay-Alfaguter Inbar , Dun Bryan , Baquero-Buitrago Jairo , Mor Adam 
Published: January 2015

Abstract
CD28 is a coreceptor expressed on T lymphocytes. Signaling downstream of CD28 promotes multiple T cell functions such as proliferation, survival, and cytokine secretion. Adhesion to APCs is another function of T cells; however, little is known with regard to the role of CD28 in this process. Our previous studies have shown that CD28 inhibits T cell adhesion, but the underlying mechanism that mediates this process remains unknown. In the present study we discovered that signaling downstream of CD28 resulted in inhibition of Rap1 activity and decreased LFA-1–mediated adhesion. We showed that this was regulated by the recruitment of calcium-promoted Ras inactivator (CAPRI), a GTPase-activating protein, to the plasma membrane downstream of CD28 signaling. CAPRI trafficking to the plasma membrane was secondary to calcium influx and was mediated by its C2A and C2B domains. We conclude that CD28 inhibits Rap1-mediated adhesion by recruiting the protein CAPRI to the plasma membrane.
A Transendocytosis Model of CTLA-4 Function Predicts Its Suppressive Behavior on Regulatory T Cells
Authors: Hou Tie Zheng , Qureshi Omar S. , Wang Chun Jing , Baker Jennifer , Young Stephen P. , Walker Lucy S. K. , Sansom David M. 
Published: January 2015

Abstract
Manipulation of the CD28/CTLA-4 pathway is at the heart of a number of immunomodulatory approaches used in both autoimmunity and cancer. Although it is clear that CTLA-4 is a critical regulator of T cell responses, the immunological contexts in which CTLA-4 controls immune responses are not well defined. In this study, we show that whereas CD80/CD86-dependent activation of resting human T cells caused extensive T cell proliferation and robust CTLA-4 expression, in this context CTLA-4 blocking Abs had no impact on the response. In contrast, in settings where CTLA-4+ cells were present as “regulators,” inhibition of resting T cell responses was dependent on CTLA-4 expression and specifically related to the number of APC. At low numbers of APC or low levels of ligand, CTLA-4–dependent suppression was highly effective whereas at higher APC numbers or high levels of ligand, inhibition was lost. Accordingly, the degree of suppression correlated with the level of CD86 expression remaining on the APC. These data reveal clear rules for the inhibitory function of CTLA-4 on regulatory T cells, which are predicted by its ability to remove ligands from APC.
Cell-Autonomous Sex Differences in Gene Expression in Chicken Bone Marrow–Derived Macrophages
Authors: Garcia-Morales Carla , Nandi Sunil , Zhao Debiao , Sauter Kristin A. , Vervelde Lonneke , McBride Derek , Sang Helen M. , Clinton Mike , Hume David A. 
Published: January 2015

Abstract
We have identified differences in gene expression in macrophages grown from the bone marrow of male and female chickens in recombinant chicken M-CSF (CSF1). Cells were profiled with or without treatment with bacterial LPS for 24 h. Approximately 600 transcripts were induced by prolonged LPS stimulation to an equal extent in the male and female macrophages. Many transcripts encoded on the Z chromosome were expressed ∼1.6-fold higher in males, reflecting a lack of dosage compensation in the homogametic sex. A smaller set of W chromosome–specific genes was expressed only in females. LPS signaling in mammals is associated with induction of type 1 IFN–responsive genes. Unexpectedly, because IFNs are encoded on the Z chromosome of chickens, unstimulated macrophages from the female birds expressed a set of known IFN-inducible genes at much higher levels than male cells under the same conditions. To confirm that these differences were not the consequence of the actions of gonadal hormones, we induced gonadal sex reversal to alter the hormonal environment of the developing chick and analyzed macrophages cultured from male, female, and female sex-reversed embryos. Gonadal sex reversal did not alter the sexually dimorphic expression of either sex-linked or IFN-responsive genes. We suggest that female birds compensate for the reduced dose of inducible IFN with a higher basal set point of IFN-responsive genes.
A Novel Model for IFN-γ–Mediated Autoinflammatory Syndromes
Authors: Reinhardt R. Lee , Liang Hong-Erh , Bao Katherine , Price April E. , Mohrs Markus , Kelly Ben L. , Locksley Richard M. 
Published: January 2015

Abstract
Autoinflammatory disease and hyperinflammatory syndromes represent a growing number of diseases associated with inappropriately controlled inflammation in multiple organs. Systemic inflammation commonly results from dysregulated activation of innate immune cells, and therapeutic targeting of the IL-1β pathway has been used to ameliorate some of these diseases. Some hyperinflammatory syndromes, however, such as hemophagocytic lymphohistiocytosis and the newly classified proteasome disability syndromes, are refractory to such treatments, suggesting that other factors or environmental stressors may be contributing. In comparing two cytokine reporter mouse strains, we identify IFN-γ as a mediator of systemic autoinflammatory disease. Chronically elevated levels of IFN-γ resulted in progressive multiorgan inflammation and two copies of the mutant allele resulted in increased mortality accompanied by myeloproliferative disease. Disease was alleviated by genetic deletion of T-bet. These studies raise the possibility that therapeutics targeting the IFN-γ pathway might be effective in hyperinflammatory conditions refractory to IL-1β–targeted therapies.
WC1 Is a Hybrid γδ TCR Coreceptor and Pattern Recognition Receptor for Pathogenic Bacteria
Authors: Hsu Haoting , Chen Chuang , Nenninger Ariel , Holz Lauren , Baldwin Cynthia L. , Telfer Janice C. 
Published: January 2015

Abstract
WC1 proteins are uniquely expressed on γδ T cells and belong to the scavenger receptor cysteine-rich (SRCR) superfamily. While present in variable, and sometimes high, numbers in the genomes of mammals and birds, in cattle there are 13 distinct genes (WC1-1 to WC1-13). All bovine WC1 proteins can serve as coreceptors for the TCR in a tyrosine phosphorylation dependent manner, and some are required for the γδ T cell response to Leptospira. We hypothesized that individual WC1 receptors encode Ag specificity via coligation of bacteria with the γδ TCR. SRCR domain binding was directly correlated with γδ T cell response, as WC1-3 SRCR domains from Leptospira-responsive cells, but not WC1-4 SRCR domains from Leptospira-nonresponsive cells, bound to multiple serovars of two Leptospira species, L. borgpetersenii, and L. interrogans. Three to five of eleven WC1-3 SRCR domains, but none of the eleven WC1-4 SRCR domains, interacted with Leptospira spp. and Borrelia burgdorferi, but not with Escherichia coli or Staphylococcus aureus. Mutational analysis indicated that the active site for bacterial binding in one of the SRCR domains is composed of amino acids in three discontinuous regions. Recombinant WC1 SRCR domains with the ability to bind leptospires inhibited Leptospira growth. Our data suggest that WC1 gene arrays play a multifaceted role in the γδ T cell response to bacteria, including acting as hybrid pattern recognition receptors and TCR coreceptors, and they may function as antimicrobials.
HIV-1–Triggered Release of Type I IFN by Plasmacytoid Dendritic Cells Induces BAFF Production in Monocytes
Authors: Gomez Alejandro M. , Ouellet Michel , Tremblay Michel J. 
Published: January 2015

AbstractHIV-1 infection leads to numerous B cell abnormalities, including hypergammaglobulinemia, nonspecific B cell activation, nonspecific class switching, increased cell turnover, breakage of tolerance, increased immature/transitional B cells, B cell malignancies, as well as a loss of capacity to generate and maintain memory, all of which contribute to a global impairment of the immune humoral compartment. Several cytokines and soluble factors, which are increased in sera of HIV-1–infected individuals, have been suggested to directly or indirectly contribute to these B cell dysfunctions, and one of these is the B cell–activating factor (BAFF). We report in this study that HIV-1 (X4- and R5-tropic) upregulates BAFF expression and secretion by human monocytes. Moreover, we show that the virus-mediated production of BAFF by monocytes relies on a type I IFN response by a small percentage of plasmacytoid dendritic cells (pDCs) present in the monocyte cultures. HIV-1–induced type I IFN by pDCs triggers BAFF production in both classical and intermediate monocytes, but not in nonclassical monocytes, which nonetheless display a very strong basal BAFF production. We report also that basal BAFF secretion was higher in monocytes obtained from females compared with those from male donors. This study provides a novel mechanistic explanation for the increased BAFF levels observed during HIV-1 infection and highlights the importance of pDC/monocyte crosstalk to drive BAFF secretion.
ChemR23, the Receptor for Chemerin and Resolvin E1, Is Expressed and Functional on M1 but Not on M2 Macrophages
Authors: Herová Magdalena , Schmid Mattia , Gemperle Claudio , Hersberger Martin 
Published: January 2015

Abstract
ChemR23 is a G protein–coupled receptor that is triggered by two ligands, the peptide chemerin and the eicosapentaenoic acid–derived lipid mediator resolvin E1 (RvE1). Chemerin acts as a chemoattractant for monocytes and macrophages, whereas RvE1 promotes resolution of inflammation-inducing macrophage phagocytosis of apoptotic neutrophils. Although ChemR23-mediated signaling plays a role in mononuclear cell migration to inflamed tissue, as well as in the resolution of inflammation, its regulation in different polarization states of macrophages is largely unknown. We analyzed the expression and function of ChemR23 in monocytes and differently activated human primary macrophages. Using 5′ RACE, we identified three transcription start sites and several splice variants of ChemR23 in both monocytes and macrophages. Although the promoters P1 and P3 are used equally in unpolarized macrophages, stimulation with LPS or IFN-γ leads to increased transcription from P3 in inflammatory M1 macrophages. Such ChemR23-expressing M1 macrophages are chemotactic to chemerin, whereas M2 macrophages not expressing ChemR23 surface receptor are not. Repolarization of ChemR23-expressing M1 macrophages with 10 nM RvE1 increases IL-10 transcription and phagocytosis of microbial particles, leading to a resolution-type macrophage distinct from the M2 phenotype. These results show that ChemR23 is tightly regulated in response to inflammatory and anti-inflammatory stimuli. The restricted expression of ChemR23 in naive and M1 macrophages supports the role of ChemR23 in the attraction of macrophages to inflamed tissue by chemerin and in the initiation of resolution of inflammation through RvE1-mediated repolarization of human M1 macrophages toward resolution-type macrophages.
High-Density IgE Recognition of the Major Grass Pollen Allergen Phl p 1 Revealed with Single-Chain IgE Antibody Fragments Obtained by Combinatorial Cloning
Authors: Madritsch Christoph , Gadermaier Elisabeth , Roder Uwe W. , Lupinek Christian , Valenta Rudolf , Flicker Sabine 
Published: January 2015

Abstract
The timothy grass pollen allergen Phl p 1 belongs to the group 1 of highly cross-reactive grass pollen allergens with a molecular mass of ∼25–30 kDa. Group 1 allergens are recognized by &gt;95% of grass pollen allergic patients. We investigated the IgE recognition of Phl p 1 using allergen-specific IgE-derived single-chain variable Ab fragments (IgE-ScFvs) isolated from a combinatorial library constructed from PBMCs of a grass pollen–allergic patient. IgE-ScFvs reacted with recombinant Phl p 1 and natural group 1 grass pollen allergens. Using synthetic Phl p 1–derived peptides, the binding sites of two ScFvs were mapped to the N terminus of the allergen. In surface plasmon resonance experiments they showed comparable high-affinity binding to Phl p 1 as a complete human IgE-derived Ab recognizing the allergens’ C terminus. In a set of surface plasmon resonance experiments simultaneous allergen recognition of all three binders was demonstrated. Even in the presence of the three binders, allergic patients’ polyclonal IgE reacted with Phl p 1, indicating high-density IgE recognition of the Phl p 1 allergen. Our results show that multiple IgE Abs can bind with high density to Phl p 1, which may explain the high allergenic activity and sensitizing capacity of this allergen.
Smad4 Promotes Differentiation of Effector and Circulating Memory CD8 T Cells but Is Dispensable for Tissue-Resident Memory CD8 T Cells
Authors: Hu Yinghong , Lee Young-Tae , Kaech Susan M. , Garvy Beth , Cauley Linda S. 
Published: January 2015

Abstract
Tissue-resident memory CD8 T cells are a unique subset of virus-specific CTLs that bolster local immune responses after becoming lodged in previously infected tissues. These cells provide enhanced protection by intercepting returning pathogens before a new infection gets established. In contrast, central memory CD8 T cells circulate in the bloodstream and proliferate in secondary lymphoid organs before replenishing effector and memory CD8 T cell populations in remote parts of the body. Both populations of virus-specific memory CD8 T cells participate in immunity to influenza virus infection; however, the signaling pathways that instruct developing memory CD8 T cells to distribute to specific tissues are poorly defined. We show that TGF-β promotes the development of pulmonary tissue-resident memory T cells via a signaling pathway that does not require the downstream signaling intermediate Sma- and Mad-related protein (Smad)4. In contrast, circulating memory CD8 T cells have no requirement for TGF-β but show signs of arrested development in the absence of Smad4, including aberrant CD103 expression. These signaling pathways alter the distribution of virus-specific CTLs in the lungs but do not prevent robust cytokine responses. Our data show that Smad4 is required for normal differentiation of multiple subsets of virus-specific CD8 T cells. In normal circumstances, Smad4 may be activated via a pathway that bypasses the TGF-β receptor. Improved understanding of these signaling pathways could be used to augment vaccine-induced immunity.
Cryptococcus neoformans–Induced Macrophage Lysosome Damage Crucially Contributes to Fungal Virulence
Authors: Davis Michael J. , Eastman Alison J. , Qiu Yafeng , Gregorka Brian , Kozel Thomas R. , Osterholzer John J. , Curtis Jeffrey L. , Swanson Joel A. , Olszewski Michal A. 
Published: January 2015

Abstract
Upon ingestion by macrophages, Cryptococcus neoformans can survive and replicate intracellularly unless the macrophages become classically activated. The mechanism enabling intracellular replication is not fully understood; neither are the mechanisms that allow classical activation to counteract replication. C. neoformans–induced lysosome damage was observed in infected murine bone marrow–derived macrophages, increased with time, and required yeast viability. To demonstrate lysosome damage in the infected host, we developed a novel flow cytometric method for measuring lysosome damage. Increased lysosome damage was found in C. neoformans–containing lung cells compared with C. neoformans–free cells. Among C. neoformans–containing myeloid cells, recently recruited cells displayed lower damage than resident cells, consistent with the protective role of recruited macrophages. The magnitude of lysosome damage correlated with increased C. neoformans replication. Experimental induction of lysosome damage increased C. neoformans replication. Activation of macrophages with IFN-γ abolished macrophage lysosome damage and enabled increased killing of C. neoformans. We conclude that induction of lysosome damage is an important C. neoformans survival strategy and that classical activation of host macrophages counters replication by preventing damage. Thus, therapeutic strategies that decrease lysosomal damage, or increase resistance to such damage, could be valuable in treating cryptococcal infections.