bluuebunny/crossref_metadata_2025_split huggingface dataset:
Les pronoms objets directs de la 3e personne et leur apport aux indices du genre grammatical dans le discours oral des enseignants en immersion
Authors: Poirier James , Lyster Roy 
Published: April 2014

Résumé: La présente étude examine la fréquence et la répartition des pronoms objets directs de la 3e personne (le, la, les, l’) ainsi que leur propension à indiquer le genre grammatical dans deux corpus oraux, l’un de 37,7 heures et l’autre de 33 heures. Le corpus principal provient du discours de six enseignants de six classes d’immersion différentes dans la région de Montréal alors que le corpus secondaire utilisé de façon complémentaire a été tiré de dialogues familiaux. Dans les deux contextes, la répartition des pronoms se lit comme suit en ordre décroissant : le > l’ > les > la. Par rapport à tous les pronoms clitiques objets directs à la 3e personne, 71 % de ceux utilisés par les enseignants et 54 % de ceux utilisés par les parents ne portent aucun indice du genre grammatical. Les résultats laissent entendre un lien possible entre le discours des enseignants et les difficultés qu’éprouvent les élèves en immersion à utiliser correctement le genre grammatical. En guise de conclusion, nous proposons des techniques pédagogiques centrées sur la forme qui mettraient l’accent sur le lien entre le genre grammatical et certaines terminaisons nominales.
Characterization of selenium and sulfur accumulation across the genus Stanleya (Brassicaceae): A field survey and common‐garden experiment
Authors: Cappa Jennifer J. , Cappa Patrick J. , El Mehdawi Ali F. , McAleer Jenna M. , Simmons Mark P. , Pilon‐Smits Elizabeth A. H. 
Published: April 2014

• Premise of study: Selenium (Se) hyperaccumulation, the capacity to concentrate the toxic element Se above 1000 mg·kg−1·dry mass, is found in relatively few taxa native to seleniferous soils. While Se hyperaccumulation has been shown to likely be an adaptation that protects plants from herbivory, its evolutionary history remains unstudied. Stanleya (Brassicaceae) is a small genus comprising seven species endemic to the western United States. Stanleya pinnata is a hyperaccumulator of selenium (Se). In this study we investigated to what extent other Stanleya taxa accumulate Se both in the field and a greenhouse setting on seleniferous soil.• Methods: We collected multiple populations of six of the seven species and all four varieties of S. pinnata. We tested leaves, fruit, and soil for in situ Se and sulfur (S) concentrations. The seeds collected in the field were used for a common garden study in a greenhouse.• Key results: We found that S. pinnata var. pinnata is the only hyperaccumulator of Se. Within S. pinnata var. pinnata, we found a geographic pattern related to Se hyperaccumulation where the highest accumulating populations are found on the eastern side of the continental divide. We also found differences in genome size within the S. pinnata species complex.• Conclusions: The S. pinnata species complex has a range of physiological properties making it an attractive system to study the evolution of Se hyperaccumulation. Beyond the basic scientific value of understanding the evolution of this fascinating trait, we can potentially use S. pinnata or its genes for environmental cleanup and/or nutrient‐enhanced dietary material.
Aneurysmal Lesions of Patients with Abdominal Aortic Aneurysm Contain Clonally Expanded T Cells
Authors: Lu Song , White John V. , Lin Wan Lu , Zhang Xiaoying , Solomides Charalambos , Evans Kyle , Ntaoula Nectaria , Nwaneshiudu Ifeyinwa , Gaughan John , Monos Dimitri S. , Oleszak Emilia L. , Platsoucas Chris D. 
Published: April 2014

Abstract
Abdominal aortic aneurysm (AAA) is a common disease with often life-threatening consequences. This vascular disorder is responsible for 1–2% of all deaths in men aged 65 years or older. Autoimmunity may be responsible for the pathogenesis of AAA. Although it is well documented that infiltrating T cells are essentially always present in AAA lesions, little is known about their role in the initiation and/or progression of the disease. To determine whether T cells infiltrating AAA lesions contain clonally expanded populations of T cells, we amplified β-chain TCR transcripts by the nonpalindromic adaptor–PCR/Vβ-specific PCR and/or Vβ-specific PCR, followed by cloning and sequencing. We report in this article that aortic abdominal aneurysmal lesions from 8 of 10 patients with AAA contained oligoclonal populations of T cells. Multiple identical copies of β-chain TCR transcripts were identified in these patients. These clonal expansions are statistically significant. These results demonstrate that αβ TCR+ T lymphocytes infiltrating aneurysmal lesions of patients with AAA have undergone proliferation and clonal expansion in vivo at the site of the aneurysmal lesion, in response to unidentified self- or nonself Ags. This evidence supports the hypothesis that AAA is a specific Ag–driven T cell disease.
Murine B-1 B Cell Progenitors Initiate B-Acute Lymphoblastic Leukemia with Features of High-Risk Disease
Authors: Montecino-Rodriguez Encarnacion , Li Katy , Fice Michael , Dorshkind Kenneth 
Published: April 2014

Abstract
B-1 and B-2 B cells derive from distinct progenitors that emerge in overlapping waves of development. The number of murine B-1 progenitors peaks during fetal development whereas B-2 B cell production predominates in adult bone marrow. Many genetic mutations that underlie B-acute lymphoblastic leukemia (B-ALL) occur in the fetus, at which time B-1 progenitor numbers are high. However, whether B-ALL can initiate in B-1 progenitors is unknown. In the present study, we report that BCR-ABL–transformed murine B-1 progenitors can be B-ALL cells of origin and demonstrate that they initiate disease more rapidly than do oncogene-expressing B-2 progenitors. We further demonstrate that B-1 progenitors exhibit relative resistance to apoptosis and undergo significant growth following oncogene expression, and we propose that these properties underlie the accelerated kinetics with which they initiate leukemia. These results provide a developmental perspective on the origin of B-ALL and indicate B cell lineage as a factor influencing disease progression.
Cutting Edge: Differential Constitutive Expression of Functional Receptors for Lysophosphatidic Acid by Human Blood Lymphocytes
Authors: Goetzl Edward J. , Kong Yvonne , Voice Julia K. 
Published: April 2014

AbstractLysophosphatidic acid (LPA) and sphingosine 1-phosphate (S1P) from platelets and macrophages mediate T cell functions. Endothelial differentiation gene-encoded G protein-coupled receptors (Edg Rs) are specific for S1P (Edg-1, -3, -5, and -8 Rs) and LPA (Edg-2, -4, and -7 Rs). Human T cell tumors express many Edg Rs for both LPA and S1P. In contrast, human blood CD4+ T cells express predominantly Edg-4, and CD8+ T cells show only traces of Edg-2 and -5, by quantification of mRNA and Edg R Ags. LPA at 10−10–10−6 M suppressed significantly the secretion of IL-2 from anti-CD3 plus anti-CD28 Ab-challenged CD4+ T cells, but not CD8+ T cells. Monoclonal anti-Edg-4 R Ab, like LPA, suppressed stimulated IL-2 secretion from CD4+ T cells, but not CD8+ T cells. Constitutive expression of Edg-4 by CD4+, but not CD8+, human T cells accounts for differential functional responsiveness of the T cell subsets to LPA.
Cutting Edge: The Tumor Counterattack Hypothesis Revisited: Colon Cancer Cells Do Not Induce T Cell Apoptosis Via the Fas (CD95, APO-1) Pathway
Authors: Favre-Felix Nathalie , Fromentin Annie , Hammann Arlette , Solary Eric , Martin François , Bonnotte Bernard 
Published: April 2014

AbstractThe counterattack hypothesis, suggesting that cancer cells express Fas ligand (FasL) and are able to kill Fas-expressing tumor-infiltrating activated T cells, was supported by reports of the killing of Jurkat cells by FasL-expressing human colon cancer cell lines. Through the use of an improved cytotoxic assay in which soluble FasL and FasL-transfected KFL9 cells were used as positive controls, we show that none of seven human colon cancer cell lines induce apoptosis of two Fas-expressing target cell lines, Jurkat and L1210-Fas cells. Moreover, in coculture experiments, cancer cell monolayers do not inhibit the growth of Fas-expressing lymphoid cells. Although FasL mRNA and protein were detected in the extracts of the colon cancer cell lines, flow cytometry and confocal microscopy failed to detect the protein on the surface of tumor cells. These results suggest that the counterattack of tumor-infiltrating T lymphocytes by cancer cells may not account for immune tolerance toward tumor cells.
Human Intestinal Epithelial Cells Express a Novel Receptor for IgA
Authors: Kitamura Tetsuro , Garofalo Roberto P. , Kamijo Atsushi , Hammond Dianne K. , Oka Janet A. , Caflisch Carlton R. , Shenoy Mohan , Casola Antonella , Weigel Paul H. , Goldblum Randall M. 
Published: April 2014

AbstractBinding and transport of polymeric Igs (pIgA and IgM) across epithelia is mediated by the polymeric Ig receptor (pIgR), which is expressed on the basolateral surface of secretory epithelial cells. Although an Fc receptor for IgA (FcαR) has been identified on myeloid cells and some cultured mesangial cells, the expression of an FcαR on epithelial cells has not been described. In this study, binding of IgA to a human epithelial line, HT-29/19A, with features of differentiated colonic epithelial cells, was examined. Radiolabeled monomeric IgA (mIgA) showed a dose-dependent, saturable, and cation-independent binding to confluent monolayers of HT-29/19A cells. Excess of unlabeled mIgA, but not IgG or IgM, competed for the mIgA binding, indicating that the binding was IgA isotype-specific and was not mediated by the pIgR. The lack of competition by asialoorosomucoid and the lack of requirement for divalent cations excluded the possibility that IgA binding to HT-29/19A cells was due to the asialoglycoprotein receptor or β-1,4-galactosyltransferase, previously described on HT-29 cells. Moreover, the FcαR (CD89) protein and message were undetectable in HT-29/19A cells. FACS analysis of IgA binding demonstrated two discrete populations of HT-29/19 cells, which bound different amounts of mIgA. IgA binding to other colon carcinoma cell lines was also demonstrated by FACS analysis, suggesting that an IgA receptor, distinct from the pIgR, asialoglycoprotein receptor, galactosyltransferase, and CD89 is constitutively expressed on cultured human enterocytes. The function of this novel IgA receptor in mucosal immunity remains to be elucidated.
Effects of Continuous Exposure to Stromal Cell-Derived Factor-1α on T Cell Rolling and Tight Adhesion to Monolayers of Activated Endothelial Cells
Authors: Kantele Jussi M. , Kurk Sandy , Jutila Mark A. 
Published: April 2014

Abstract
Immobilized stromal cell-derived factor-1α (SDF-1α) has been shown to induce tight adhesion of T cells to purified ICAM-1 in assays done under flow conditions. In this study, we show that soluble SDF-1α induced a rapid (within 20 s) cessation of rolling and tight adhesion of &gt;90% of the rolling T cells on monolayers of activated endothelial cells under similar flow. Within 4 min, the T cells had either started to migrate between the endothelial cells or re-entered the rolling and circulating lymphocyte pool. This deadherence of the firmly bound cells, with either ensuing transmigration or continued rolling, was most likely due to desensitization of lymphocytes to the continuously present SDF-1α. The released rolling lymphocytes could still respond to other activating signals by a second round of tight adhesion. Pretreating the lymphocytes with pertussis toxin almost completely blocked the effect of the chemokine, confirming that the induction of firm adhesion was due to the function of the chemokine on the lymphocytes and not the endothelial cells. Pretreating the endothelium with SDF-1α did not lead to firm adhesion of subsequently added lymphocytes, also indicating that the effect was due to soluble, not endothelially bound, chemokine. Blocking experiments showed that the same molecules mediated rolling before and after SDF-1α-induced tight adhesion. This is the first study to demonstrate the effect of soluble SDF-1α on T cell rolling on an endothelial cell monolayer. The data broaden our understanding of the stimulatory factors directing the firm adhesion and ensuing transmigration of leukocytes into tissues through activated endothelium.
Engagement of CD4 Before TCR Triggering Regulates Both Bax- and Fas (CD95)-Mediated Apoptosis
Authors: Somma Francesca , Tuosto Loretta , Montani Maria Saveria Gilardini , Di Somma M. Maddalena , Cundari Enrico , Piccolella Enza 
Published: April 2014

AbstractIn the present study, we have aimed at clarifying the CD4-dependent molecular mechanisms that regulate human memory T cell susceptibility to both Fas (CD95)-dependent and Bcl-2-dependent apoptotic pathways following antigenic challenge. To address this issue, we used an experimental system of viral and alloantigen-specific T cell lines and clones and two ligands of CD4 molecules, Leu-3a mAb and HIV gp120. We demonstrate that CD4 engagement before TCR triggering suppresses the TCR-mediated neosynthesis of the Flice-like inhibitory protein and transforms memory T cells from a CD95-resistant to a CD95-susceptible phenotype. Moreover, evidence that the apoptotic programs were executed while Fas ligand mRNA expression was inhibited led us to analyze Bcl-2-dependent pathways. The data show that the engagement of CD4 separately from TCR influences the expression of the proapoptotic protein Bax independently of the anti-apoptotic protein Bcl-2, whereas Ag activation coordinately modulates both Bax and Bcl-2. The increased expression of Bax and the consequent dissipation of the mitochondrial transmembrane potential (ΔΨm) suggest a novel immunoregulatory function of CD4 and demonstrate that both passive cell death and activation-induced cell death are operative in CD4+ memory T cells. Furthermore, analysis of the mechanisms by which IL-2 and IL-4 cytokines exert their protective function on CD4+ T cells in the presence of soluble CD4 ligands shows that they were able to revert susceptibility to Bax-mediated but not to CD95-dependent apoptotic pathways.
κ-Opioid Regulation of Thymocyte IL-7 Receptor and C-C Chemokine Receptor 2 Expression
Authors: Zhang Lily , Rogers Thomas J. 
Published: April 2014

AbstractEndogenous and exogenous κ-opioid agonists have been widely reported to modulate the immune response. We have published results that show that the superantigen-induced proliferative response of thymocytes is inhibited by the selective κ-opioid agonist trans-3,4-dichloro-N-methyl-N-[2-(1-pyrolidinyl)cyclohexyl]benzeneaceamide methanesulfonate (U50,488H). Previous work has established that the κ-opioid receptor is widely expressed within the thymus; however, little is known about the role of the κ-opioid receptor in the function of thymocytes. In the present report, we have examined the impact of U50,488H administration on the expression of cytokines in superantigen-stimulated thymocytes by RNase protection analysis. We have measured detectable levels of the cytokines IL-2, IL-4, IL-5, IL-13, and IFN-γ, and the chemokines lymphotactin and RANTES, in stimulated thymocyte cultures; however, addition of U50,488H did not alter the expression of these cytokines. Examination of cytokine receptor expression by these thymocytes revealed a significant inhibition in the expression of the transcript for the IL-7 receptor α-chain (IL-7Rα), and these results were confirmed by flow cytometry. Surprisingly, the expression of several other cytokine receptor chains including the common γ-chain, IL-2Rβ, or the IL-2Rα, IL-4Rα, and IL-15Rα chains, was not altered. In contrast to these results, a significant elevation in the expression of the chemokine receptor CCR2 was observed in U50,488H-treated cultures. These results suggest that the κ-opioid receptor may function to promote cellular migration at the expense of the sensitivity to the growth-promoting/maturation activity of IL-7.
Phagosomes Acquire Nascent and Recycling Class II MHC Molecules but Primarily Use Nascent Molecules in Phagocytic Antigen Processing
Authors: Ramachandra Lakshmi , Harding Clifford V. 
Published: April 2014

AbstractPhagosomes contain class II MHC (MHC-II) and form peptide:MHC-II complexes, but the source of phagosomal MHC-II molecules is uncertain. Phagosomes may acquire nascent MHC-II or preexisting, recycling MHC-II that may be internalized from the plasma membrane. Brefeldin A (BFA) was used to deplete nascent MHC-II in murine macrophages to determine the relative contributions of nascent and recycling MHC-II molecules to phagocytic Ag processing. In addition, biotinylation of cell-surface proteins was used to assess the transport of MHC-II from the cell surface to phagosomes. BFA inhibited macrophage processing of latex bead-conjugated Ag for presentation to T cells, suggesting that nascent MHC-II molecules are important in phagocytic Ag processing. Furthermore, detection of specific peptide:MHC-II complexes in isolated phagosomes confirmed that BFA decreased formation of peptide:MHC-II complexes within phagosomes. Both flow organellometry and Western blot analysis of purified phagosomes showed that about two-thirds of phagosomal MHC-II was nascent (depleted by 3 h prior treatment with BFA) and primarily derived from intracellular sites. About one-third of phagosomal MHC-II was preexisting and primarily derived from the plasma membrane. BFA had little effect on phagosomal H2-DM or the degradation of bead-associated Ag. Thus, inhibition of phagocytic Ag processing by BFA correlated with depletion of nascent MHC-II in phagosomes and occurred despite the persistent delivery of plasma membrane-derived recycling MHC-II molecules and other Ag-processing components to phagosomes. These observations suggest that phagosomal Ag processing depends primarily on nascent MHC-II molecules delivered from intracellular sites, e.g., endocytic compartments.
Granulocyte/Macrophage Colony-Stimulating Factor Inhibits IL-12 production of Mouse Langerhans Cells
Authors: Tada Yayoi , Asahina Akihiko , Nakamura Koichiro , Tomura Michio , Fujiwara Hiromi , Tamaki Kunihiko 
Published: April 2014

AbstractWe investigated the capacity of mouse Langerhans cells (LC) to produce IL-12, a central cytokine in a Th1 type of immune responses. We prepared purified LC (&gt;95%) from BALB/c mouse skin by the panning method using anti-I-Ad mAb. An ELISA showed that purified LC spontaneously produced IL-12 p40, and that its production was up-regulated following simultaneous stimulation with anti-CD40 mAb and IFN-γ. Surprisingly, GM-CSF strikingly inhibited IL-12 p40 production by anti-CD40/IFN-γ-stimulated LC (% inhibition = 97.0 ± 0.9% at 1 ng/ml GM-CSF). Supernatants of 48-h cultured keratinocytes (KC) also caused the inhibition of LC IL-12 p40 secretion, and this effect was neutralized by anti-GM-CSF mAb. IL-1α (1 ng/ml)-stimulated KC produced much more GM-CSF than unstimulated KC (60.9 ± 0.2 pg/ml vs 20.9 ± 1.7 pg/ml), and IL-1α-stimulated KC supernatants strongly inhibited IL-12 p40 production by anti-CD40/IFN-γ-stimulated LC (% inhibition = 89.4 ± 1.4%). A bioassay using an IL-12-dependent T cell line demonstrated the correlation of the level of IL-12 p40 with the bioactivity of IL-12. These results provide important implications for the pathogenesis of atopic dermatitis, which involves the participation of LC and KC with the capacity to produce IL-12 and GM-CSF, respectively.
A New Look at Syk in αβ and γδ T Cell Development Using Chimeric Mice with a Low Competitive Hematopoietic Environment
Authors: Colucci Francesco , Guy-Grand Delphine , Wilson Anne , Turner Martin , Schweighoffer Edina , Tybulewicz Victor L. J. , Di Santo James P. 
Published: April 2014

AbstractThe Syk protein tyrosine kinase (PTK) is essential for B, but not T or NK, cell development, although certain T cell subsets (i.e., γδ T cells of intestine and skin) appear to be dependent on Syk. In this report, we have re-evaluated the role of Syk in T cell development in hematopoietic chimeras generated by using Syk-deficient fetal liver hematopoietic stem cells (FL-HSC). We found that Syk−/− FL-HSC were vastly inferior to wild-type FL-HSC in reconstituting T cell development in recombinant-activating gene 2 (RAG2)-deficient mice, identifying an unexpected and nonredundant role for Syk in this process. This novel function of Syk in T cell development was mapped to the CD44−CD25+ stage. According to previous reports, development of intestinal γδ T cells was arrested in Syk−/− →RAG2−/− chimeras. In striking contrast, when hosts were the newly established alymphoid RAG2 × common cytokine receptor γ-chain (RAG2/γc) mice, Syk−/− chimeras developed intestinal γδ T cells as well as other T cell subsets (including αβ T cells, NK1.1+ αβ T cells, and splenic and thymic γδ T cells). However, all Syk-deficient T cell subsets were reduced in number, reaching about 25–50% of controls. These results attest to the utility of chimeric mice generated in a low competitive hematopoietic environment to evaluate more accurately the impact of lethal mutations on lymphoid development. Furthermore, they suggest that Syk intervenes in early T cell development independently of ZAP-70, and demonstrate that Syk is not essential for the intestinal γδ T cell lineage to develop.
Differential Requirement for p56lck in HIV-tat Versus TNF-Induced Cellular Responses: Effects on NF-κB, Activator Protein-1, c-Jun N-Terminal Kinase, and Apoptosis
Authors: Manna Sunil K. , Aggarwal Bharat B. 
Published: April 2014

Abstract
HIV-tat protein, like TNF, activates a wide variety of cellular responses, including NF-κB, AP-1, c-Jun N-terminal kinase (JNK), and apoptosis. Whether HIV-tat transduces these signals through the same mechanism as TNF is not known. In the present study we investigated the role of the T cell-specific tyrosine kinase p56lck in HIV-tat and TNF-mediated cellular responses by comparing the responses of Jurkat T cells with JCaM1 cells, an isogeneic lck-deficient T cell line. Treatment with HIV-tat protein activated NF-κB, degraded IκBα, and induced NF-κB-dependent reporter gene expression in a time-dependent manner in Jurkat cells but not in JCaM1 cells, suggesting the critical role of p56lck kinase. These effects were specific to HIV-tat, as activation of NF-κB by PMA, LPS, H2O2, and TNF was minimally affected. p56lck was also found to be required for HIV-tat-induced but not TNF-induced AP-1 activation. Similarly, HIV-tat activated the protein kinases JNK and mitogen-activated protein kinase kinase in Jurkat cells but not in JCaM1 cells. HIV-tat also induced cytotoxicity, activated caspases, and reactive oxygen intermediates in Jurkat cells, but not in JCaM1 cells. HIV-tat activated p56lck activity in Jurkat cells. Moreover, the reconstitution of JCaM1 cells with p56lck tyrosine kinase reversed the HIV-tat-induced NF-κB activation and cytotoxicity. Overall, our results demonstrate that p56lck plays a critical role in the activation of NF-κB, AP-1, JNK, and apoptosis by HIV-tat protein but has minimal or no role in activation of these responses by TNF.