bluuebunny/crossref_metadata_2025_split huggingface dataset:
Tethering of Ficolin-1 to cell surfaces through recognition of sialic acid by the fibrinogen-like domain
Authors: Honoré Christian , Rørvig Sara , Hummelshøj Tina , Skjoedt Mikkel-Ole , Borregaard Niels , Garred Peter 
Published: April 2010

Abstract
Molecular mechanism behind Ficolin-1 association with leukocytes.
Three Ficolins have been identified in humans: Ficolin-1 (M-Ficolin), Ficolin-2 (L-Ficolin), and Ficolin-3 (H-Ficolin). Ficolin-1 is the least-described of the Ficolins and is expressed by monocytes, granulocytes, and in the lungs. Ficolin-1 is found circulating at low concentrations in serum but is regarded primarily as a secretory molecule that exerts its function locally in inflamed tissues. Ficolin-1 has been reported on the surface of monocytes and granulocytes and was suggested originally to function as a phagocytic receptor. However, the molecule does not contain any obvious transmembrane domain, and no binding partners have been identified. To gain further insight in the physiological role of Ficolin-1, we sought to identify the molecular mechanism responsible for the membrane association of Ficolin-1 to monocytes and granulocytes. We demonstrate that expression of Ficolin-1 on the cell surface is restricted to monocytes and granulocytes. Ficolin-1 is tethered to the cell surface of these cells through its fibrinogen-like domain, and the ligand involved in the binding of Ficolin-1 is shown to be sialic acid. Moreover, rFicolin-1 bound activated but not resting T lymphocytes. Together, these results demonstrate a novel self-recognition mechanism of leukocytes mediated by the fibrinogen-like domain of Ficolin-1.
Postprandial bone turnover is independent of calories above 250 kcal
Authors: Elnenaei Manal O , Musto Rebecca , Alaghband-Zadeh Jamshid , Moniz Caje , Le Roux Carel W 
Published: April 2010

Background The mechanisms causing bone turnover after food intake have not yet been elucidated. Several gut hormones are secreted in the postprandial phase, proportional to meal calorie content, and possibly one or more of these could influence bone turnover. The aim of this study was to investigate bone turnover in proportion to graded-calorie and fixed calcium containing meals. Methods A group of healthy volunteers were given six meals with calories varying from 250 to 3000 kcal on different occasions. All the meals contained 500 mg of calcium. C-telopeptide type I collagen (CTX) was measured before and 180 min after each meal. Results All meals significantly reduced CTX between 35.8 ± 5.6% and 44.8 ± 3.8%. No significant difference in CTX was however apparent for the different calorie containing meals. Observed differences suggest a trend to greater CTX suppression with lower protein and higher fat content of meals. Conclusion Changes in CTX are not proportional to calorie contents when the meals contain 500 mg of calcium. Further studies should now determine whether patients with increased bone resorption would benefit from multiple small meals to slow down the rate of bone loss.
Temperature Variation in Energy Absorption System Functionalized by Nanomaterials
Authors: Qiao Yu , Sun Zhongyuan , Lu Weiyi , Han Aijie 
Published: April 2010

AbstractThe thermal effect on the nanofluidic behaviors in a nanoporous silica gel is investigated experimentally. When a nanoporous silica gel is modified by silyl groups, its surface becomes hydrophobic. A sufficiently high external pressure must be applied to overcome the capillary effect; otherwise liquid infiltration could not occur. The formation and the disappearance of a solid–liquid interface are employed for energy storage or dissipation. When the hydrophobic surface of nanoporous silica gel is decomposed at various temperatures, the organic surface layers can be deactivated. As a result, the degree of hydrophobicity, which can be measured by the liquid infiltration pressure, is lowered. The infiltration and defiltration behaviors of liquid are dependent on the controlled by the decomposition-treatment temperature.
Fabrication of Permalloy Particles by Pulsed Laser Ablation in Water and Tween 80 Aqueous Solution
Authors: Yan Zijie , Bao Ruqiang , Dinu Cerasela Z , Chrisey Douglas B 
Published: April 2010

AbstractPermalloy particles were fabricated by pulsed excimer laser ablation in distilled water and Tween 80 aqueous solution with the same laser parameters. Nearly spherical particles and irregular and porous fragments were obtained in water due to rapid condensation and growth of the laser ablated clusters. The products obtained in Tween 80 aqueous solution contained well-shaped spheres but some were laser sintered together via laser-particle interactions. Holes or pits were observed on the surface of some particles, which we consider were caused by laser induced bubbles in the liquid. Our results demonstrate the rich environment ablation in liquids can be for novel particle formation.
Effects of acid treatment duration and sulfuric acid molarity on purification of multi-walled carbon nanotubes
Authors: Mortazavi Seyedeh , Novinrooz Abdul , Reyhani Ali , Mirershadi Soghra 
Published: April 2010

AbstractMulti-walled carbon nanotubes were synthesized using a Fe-Ni bimetallic catalyst supported by MgO using thermal chemical vapor deposition. Purification processes to remove unwanted carbon structures and other metallic impurities were carried out by boiling in sulfuric acid solution. Various analytical techniques such as TGA/DSC, Raman spectroscopy, SEM, HRTEM and EDAX were employed to investigate the morphology, graphitization and quality of the carbon nanotubes. The obtained results reveal the molarity of sulfuric acid and immersed time of the carbon nanotubes in the acid solution is very effective at purifying multi-walled carbon nanotubes. It was also found that 5 M concentration of boiling sulfuric acid for a 3 h treatment duration led to the highest removal of the impurities with the least destructive effect. Moreover, it was observed that acid treatment results in decreasing of CNTs’ diameter.
Inoculation with a bacterial consortium alleviates the effect of cadmium overdose in soybean plants
Authors: Zaets Iryna , Kramarev Sergij , Kozyrovska Natalia 
Published: April 2010

Abstract
Inoculating plants that have inefficient antioxidant systems with plant-associated bacteria allows them to overcome heavy metal intoxication. We monitored protein oxidation, the activity of plant defense system enzymes, and the phenolics content in soybean (Glycine max L.) during a prolonged exposure to cadmium (Cd). The assistance of the bacterial consortium reduced the bioavailability of Cd in a soil containing 10 times the metal’s Standard Maximum Value (SMV). This reduced the accumulation of Cd in the soybeans’ roots and seeds. At 100 SMV, bacterial inoculation resulted in increased Cd bioavailability, which enhanced cadmium uptake by the soybean plants. At both Cd concentrations, oxidative stress was more prolonged in the soybean’s roots than its leaves. In cadmium-polluted soil, glutathion peroxidase activity changed more rapidly in the roots of plants when they had been inoculated. Inhibition of the peroxidases’ activities strengthened the activity of glutathione-S-transferase; increased the phenolics content in plant roots; and alleviated stress in inoculated soybean plants compared to untreated plants. The bacterial consortium may be recommended for a plant protection at 10 SMV Cd in the soil, and for phytostabilization at 100 SMV.
Synergy between Salvia officinalis L. and some preservatives
Authors: Stanojević Dragana , Čomić Ljiljana , Stefanović Olgica 
Published: April 2010

Abstract
The aim of the present study is to investigate the antibacterial activity of Salvia officinalis L. aqueous extracts and its synergistic action with preservatives sodium nitrite, sodium benzoate and potassium sorbate in vitro against selected food spoiling bacteria. Synergy was assessed by the checkerboard assay method and quantitatively represented by the FIC index. Synergistic action was established for aqueous extract/ sodium benzoate, aqueous extract/ potassium sorbate, aqueous extract/ sodium nitrite combinations. Synergy was detected in relation to: Agrobacterium tumefaciens, Bacillus subtilis and Proteus sp. Synergy was established at plant extract and preservative concentrations corresponding up to 1/8 MIC values.
Calcium-Activated Pathways and Oxidative Burst Mediate Zymosan-Induced Signaling and IL-10 Production in Human Macrophages
Authors: Kelly Erin K. , Wang Lu , Ivashkiv Lionel B. 
Published: April 2010

AbstractOutside of the TLR paradigm, there is little understanding of how pathogen recognition at the cell surface is linked to functional responses in cells of the innate immune system. Recent work in this area demonstrates that the yeast particle zymosan, by binding to the β-glucan receptor Dectin-1, activates an ITAM-Syk–dependent pathway in dendritic cells, which is required for optimal cytokine production and generation of an oxidative burst. It remains unclear how activation of Syk is coupled to effector mechanisms. In human macrophages, zymosan rapidly activated a calcium-dependent pathway downstream of Dectin-1 and Syk that led to activation of calmodulin-dependent kinase II and Pyk2. Calmodulin-dependent kinase and Pyk2 transduced calcium signals into activation of the ERK–MAPK pathway, CREB, and generation of an oxidative burst, leading to downstream production of IL-10. These observations identify a new calcium-mediated signaling pathway activated by zymosan and link this pathway to both inflammatory and anti-inflammatory responses in macrophages.
Murine Kupffer Cells Are Protective in Total Hepatic Ischemia/Reperfusion Injury with Bowel Congestion through IL-10
Authors: Ellett Justin D. , Atkinson Carl , Evans Zachary P. , Amani Zainab , Balish Edward , Schmidt Michael G. , van Rooijen Nico , Schnellmann Rick G. , Chavin Kenneth D. 
Published: April 2010

Abstract
Kupffer cells (KCs) are thought to mediate hepatocyte injury via their production of proinflammatory cytokines and reactive oxygen species in response to stress. In this study, we depleted KCs from the liver to examine their role in total warm hepatic ischemia/reperfusion (I/R) injury with bowel congestion. We injected 8-wk-old C57BL/10J mice with liposome-encapsulated clodronate 48 h before 35 min of hepatic ischemia with bowel congestion, followed by 6 or 24 h of reperfusion. KC-depleted animals had a higher mortality rate than diluent-treated animals and a 10-fold elevation in transaminase levels that correlated with increases in centrilobular necrosis. There was extensive LPS binding to the endothelial cells, which correlated with an upregulation of endothelial adhesion molecules in the KC-depleted animals versus diluent-treated animals. There was an increase in the levels of proinflammatory cytokines in KC-depleted animals, and a concomitant decrease in IL-10 levels. When KC-depleted mice were treated with recombinant IL-10, their liver damage profile in response to I/R was similar to diluent-treated animals, and endothelial cell adhesion molecules and proinflammatory cytokine levels decreased. KCs are protective in the liver subjected to total I/R with associated bowel congestion and are not deleterious as previously thought. This protection appears to be due to KC secretion of the potent anti-inflammatory cytokine IL-10.
TCR Stimulation Drives Cleavage and Shedding of the ITIM Receptor CD31
Authors: Fornasa Giulia , Groyer Emilie , Clement Marc , Dimitrov Jordan , Compain Caroline , Gaston Anh-Thu , Varthaman Aditi , Khallou-Laschet Jamila , Newman Debra K. , Graff-Dubois Stéphanie , Nicoletti Antonino , Caligiuri Giuseppina 
Published: April 2010

Abstract
CD31 is a transmembrane molecule endowed with T cell regulatory functions owing to the presence of 2 immunotyrosine-based inhibitory motifs. For reasons not understood, CD31 is lost by a portion of circulating T lymphocytes, which appear prone to uncontrolled activation. In this study, we show that extracellular T cell CD31 comprising Ig-like domains 1 to 5 is cleaved and shed from the surface of human T cells upon activation via their TCR. The shed CD31 can be specifically detected as a soluble, truncated protein in human plasma. CD31 shedding results in the loss of its inhibitory function because the necessary cis-homo–oligomerization of the molecule, triggered by the trans-homophilic engagement of the distal Ig-like domain 1, cannot be established by CD31shed cells. However, we show that a juxta-membrane extracellular sequence, comprising part of the domain 6, remains expressed at the surface of CD31shed T cells. We also show that the immunosuppressive CD31 peptide aa 551–574 is highly homophilic and possibly acts by homo-oligomerizing with the truncated CD31 remaining after its cleavage and shedding. This peptide is able to sustain phosphorylation of the CD31 ITIM686 and of SHP2 and to inhibit TCR-induced T cell activation. Finally, systemic administration of the peptide in BALB/c mice efficiently suppresses Ag-induced T cell-mediated immune responses in vivo. We conclude that the loss of T cell regulation caused by CD31 shedding driven by TCR stimulation can be rescued by molecular tools able to engage the truncated juxta-membrane extracellular molecule that remains exposed at the surface of CD31shed cells.
CD40 Signaling in CD8+CD40+ T Cells Turns On Contra-T Regulatory Cell Functions
Authors: Martin Sunil , Pahari Sushmita , Sudan Raki , Saha Bhaskar 
Published: April 2010

Abstract
CD4+ regulatory T cells (Treg cells) mediate immunosuppression, whereas CD8+ T cells confer resistance in many diseases. It is unknown whether CD8+ T cells confer protection by antagonizing the Treg cells. Using a model of stage-specific immune responses against Leishmania donovani infection in susceptible BALB/c mice, we report that CD3+CD8+CD40+ T cells executed CD40-dependent cytotoxicity on CD3+CD4+CD127dimGITR+CD25+ Treg cells during the initial phase of the infection but were later apoptosed by IL-10. CD40 signaled through Ras, PI3K, and protein kinase C, resulting in p38MAPK- or ERK-1/2–independent, but NF-κB–dependent, induction of the cytotoxic mediators granzyme and perforin. Adoptive transfer of CD3+CD8+CD40+ T cells reduced the L. donovani infection in BALB/c mice. These results identify CD3+CD8+CD40+ T cells as the contra-Treg cells and imply a novel immunotherapeutic principle.
Combination Therapy of Established Tumors by Antibodies Targeting Immune Activating and Suppressing Molecules
Authors: Takeda Kazuyoshi , Kojima Yuko , Uno Tomoyasu , Hayakawa Yoshihiro , Teng Michele W. L. , Yoshizawa Hirohisa , Yagita Hideo , Gejyo Fumitake , Okumura Ko , Smyth Mark J. 
Published: April 2010

Abstract
The blockade of immune suppression against antitumor responses is a particularly attractive strategy when combined with agents that promote tumor-specific CTLs. In this study, we have attempted to further improve the CTL induction and potent antitumor efficacy of a combination mAb-based therapy (termed “trimAb therapy”) that comprises tumor cell death-inducing anti-death receptor 5 mAb and immune activating anti-CD40 and anti-CD137 mAbs. Among trimAb-treated tumors, the infiltration of CD4+ Foxp3+ cells was greater in progressing tumors compared with stable tumors. Blockade of CTLA-4 (CD152)-mediated signals by an antagonistic mAb substantially increased the tumor rejection rate of trimAb therapy, although the immune responses of draining lymph node cells were not augmented. Interestingly, by comparison, additional treatment with agonistic anti-glucocorticoid-induced TNF receptor mAb, antagonistic anti-programmed death-1 (CD279) mAb, or agonistic anti-OX40 (CD134) mAb significantly augmented immune responses of draining lymph node cells, but did not augment the therapeutic effect of trimAb. CD4 T cell depletion reduced the antitumor effect of anti–CTLA-4 mAb treatment alone, but did not reduce the tumor rejection rate of trimAb in conjunction with anti–CTLA-4 mAb. Thus, the blockade of the CTLA-4–mediated inhibitory signal in tumor infiltrating CTL may be the most effective strategy to augment the effect of immune therapies that generate tumor-specific CTL.
CD4+ T Cells Elicit Host Immune Responses to MHC Class II− Ovarian Cancer through CCL5 Secretion and CD40-Mediated Licensing of Dendritic Cells
Authors: Nesbeth Yolanda C. , Martinez Diana G. , Toraya Seiko , Scarlett Uciane K. , Cubillos-Ruiz Juan R. , Rutkowski Melanie R. , Conejo-Garcia Jose R. 
Published: April 2010

Abstract
T cell adoptive transfer strategies that have produced clinical remissions against specific tumors have so far produced disappointing results against ovarian cancer. Recent evidence suggests that adoptively transferred CD4+ T cells can trigger endogenous immune responses in particular patients with ovarian cancer through unknown mechanisms. However, conflicting reports suggest that ovarian cancer-infiltrating CD4+ T cells are associated with negative outcomes. In this study, we elucidate the phenotypic attributes that enable polyclonal CD4+ T cells briefly primed against tumor Ags to induce therapeutically relevant endogenous antitumor immune responses. Our results unveil a therapeutic mechanism whereby tumor-primed CD4+ T cells transferred into ovarian cancer-bearing mice secrete high levels of CCL5, which recruits endogenous CCR5+ dendritic cells to tumor locations and activate them through CD40–CD40L interactions. These newly matured dendritic cells are then able to prime tumor-specific endogenous CD8+ T cells, which mediate long-term protection. Correspondingly, administration of tumor-primed CD4+ T cells significantly delayed progression of MHC class II− ovarian cancers, similarly to CD8+ T cells only, and directly activated wild-type but not CD40-deficient dendritic cells recruited to the tumor microenvironment. Our results unveil a CCL5- and CD40L-dependent mechanism of transferring immunity from exogenously activated CD4+ T cells to tumor-exposed host cells, resulting in sustained antitumor effects. Our data provide a mechanistic rationale for incorporating tumor-reactive CD4+ T cells in adoptive cell transfer immunotherapies against ovarian cancer and underscore the importance of optimizing immunotherapeutic strategies for the specific microenvironment of individual tumors.
The Mandatory Role of IL-10–Producing and OX40 Ligand-Expressing Mature Langerhans Cells in Local UVB-Induced Immunosuppression
Authors: Yoshiki Ryutaro , Kabashima Kenji , Sakabe Jun-ichi , Sugita Kazunari , Bito Toshinori , Nakamura Motonobu , Malissen Bernard , Tokura Yoshiki 
Published: April 2010

AbstractThe mechanism underlying the local UVB-induced immunosuppression is a central issue to be clarified in photoimmunology. There have been reported a considerable number of cells and factors that participate in the sensitization phase-dependent suppression, including Langerhans cells (LCs), regulatory T cells, IL-10, and TNF-α. The recent important finding that LC-depleted mice rather exhibit enhanced contact hypersensitivity responses urged us to re-evaluate the role of LCs along with dermal dendritic cells (dDCs) in the mechanism of UVB-induced immunosuppression. We studied the surface expression of OX40 ligand (OX40L) and the intracellular expression of IL-10 in LCs and dDCs from UVB-irradiated (300 mJ/cm2) skin of BALB/c mice and those migrating to the regional lymph nodes from UVB-irradiated, hapten-painted mice. In epidermal and dermal cell suspensions prepared from the UVB-irradiated skin, LCs expressed OX40L as well as CD86 and produced IL-10 at a higher level than Langerin‒ dDCs. The UVB-induced immunosuppression was attenuated by the administration of IL-10–neutralizing or OX40L-blocking Abs. In mice whose UVB-irradiated, hapten-painted skin was dissected 1 d after hapten application, the contact hypersensitivity response was restored, because this treatment allowed dDCs but not LCs to migrate to the draining lymph nodes. Moreover, LC-depleted mice by using Langerin-diphtheria toxin receptor–knocked-in mice showed impaired UVB-induced immunosuppression. These results suggest that IL-10–producing and OX40L-expressing LCs in the UVB-exposed skin are mandatory for the induction of Ag-specific regulatory T cells.
Prostaglandin I2–IP Signaling Promotes Th1 Differentiation in a Mouse Model of Contact Hypersensitivity
Authors: Nakajima Saeko , Honda Tetsuya , Sakata Daiji , Egawa Gyohei , Tanizaki Hideaki , Otsuka Atsushi , Moniaga Catharina Sagita , Watanabe Takeshi , Miyachi Yoshiki , Narumiya Shuh , Kabashima Kenji 
Published: April 2010

Abstract
PGI2, which exerts its actions via its specific Gs-coupled I prostanoid receptor (IP), is known to be present in the lymph nodes, but its roles in acquired cutaneous immune responses remain unclear. To investigate the role of PGI2–IP signaling in cutaneous immune responses, we applied IP-deficient (Ptgir−/−) mice to contact hypersensitivity as a model of acquired immune response and found that Ptgir−/− mice exhibited a significantly decreased contact hypersensitivity response. Lymph node cells from sensitized Ptgir−/− mice exhibited decreased IFN-γ production and a smaller T-bet+ subset compared with control mice. PGI synthase and IP expression were detected in dendritic cells and T cells, respectively, by quantitative real-time PCR analysis, suggesting that PGI2 produced by dendritic cells acts on IP in T cells. In fact, in vitro Th1 differentiation was enhanced by an IP agonist, and this enhancement was nullified by protein kinase A inhibitor. These results suggest that PGI2–IP signaling promotes Th1 differentiation through a cAMP-protein kinase A pathway and thereby initiates acquired cutaneous immune responses.
Resistance to Dengue Virus Infection in Mice Is Potentiated by CXCL10 and Is Independent of CXCL10-Mediated Leukocyte Recruitment
Authors: Ip Peng-Peng , Liao Fang 
Published: April 2010

AbstractCXCL10 is an IFN-inducible chemokine ligand that binds CXCR3, a receptor that is expressed on lymphocytes; CXCL10 shares the CXCR3 receptor with another two ligands, CXCL9 and CXCL11. Previously, we found that CXCL10−/− mice were more susceptible than wild-type (WT) mice to dengue virus (DENV) infection. In this study, we explored the mechanisms underlying this enhanced susceptibility. We found that viral loads were higher in the brains of CXCL10−/− mice than in WT mice. Presuming a defect in effector lymphocyte migration, we investigated whether recruitment of effector T cells and Ab-secreting cells to the infected tissues were impaired in CXCL10−/− mice. Unexpectedly, compared with WT, CXCL10−/− mice had comparable numbers of total infiltrating T cells, higher numbers of CXCR3+ T cells, and higher numbers of Ab-secreting cells in the brain. Additionally, we found that CXCL10 was induced in neurons following DENV infection and that CXCL10 competed with DENV for binding to cell surface heparan sulfate, a coreceptor for DENV entry, thus inhibiting binding of DENV to neuronal cells. These results demonstrate that the enhanced susceptibility of CXCL10−/− mice to DENV infection is not due to a defect in recruitment of effector lymphocytes but rather to an antiviral activity that promotes viral clearance.
CpG Inhibits Pro-B Cell Expansion through a Cathepsin B-Dependent Mechanism
Authors: Lalanne Ana Inés , Moraga Ignacio , Hao Yi , Pereira João Pedro , Alves Nuno L. , Huntington Nicholas D. , Freitas Antonio A. , Cumano Ana , Vieira Paulo 
Published: April 2010

AbstractTLR9 is expressed in cells of the innate immune system, as well as in B lymphocytes and their progenitors. We investigated the effect of the TLR9 ligand CpG DNA on the proliferation of pro-B cells. CpG DNA inhibits the proliferation of pro-B, but not pre-B, cells by inducing caspase-independent cell death through a pathway that requires the expression of cathepsin B. This pathway is operative in Rag-deficient mice carrying an SP6 transgene, in which B lymphopoiesis is compromised, to reduce the size of the B lymphocyte precursor compartments in the bone marrow. Thus, TLR9 signals can regulate B lymphopoiesis in vivo.