bluuebunny/crossref_metadata_2025_split huggingface dataset:
Long‐term temporal changes of plant phenology in the Western Mediterranean
Authors: GORDO OSCAR , SANZ JUAN JOSÉ 
Published: January 2009

AbstractPlants are altering their life cycles in response to current climatic change around the globe. More than 200 000 records for six phenological events (leaf unfolding, flowering, fruit ripening, fruit harvesting, leaf falling and growing season) of 29 perennial species for the period 1943–2003 recorded throughout Spain provide the longest temporal and the broadest spatial assessment of plant phenology changes in the Mediterranean region. The overwhelming majority of the 118 studied phenophases shifted their dates in recent decades. Such changes differed among phenological events. Leaf unfolding, flowering and fruiting are markedly advancing (−0.48, −0.59 and −0.32 days yr−1, respectively), but only since the mid‐1970s. Anemophilous have advanced more days their flowering than entomophilous. However, some species have delayed and others have advanced their leaf falling dates and as a result only a weak shift was observed in this event for the whole of the studied species (+0.12 days yr−1). The growing season lengthened by 18 days, which implies an increase of 8% in the life of annual leaves. Such an increase was achieved mainly through the advance of leaf unfolding dates in the spring, one of the most productive times of year for vegetation in the Mediterranean. Shifts in the plant calendar were accompanied as well by long‐term changes in the range of onset dates in 39% of studied phenophases. Leaf unfolding, flowering and growing season tended to reduce spatial variability, reflecting a faster and more synchronized onset (or duration) of phenophases across the study area. Changes in spatial variability may aggravate calendar mismatching with other trophic levels resulting from changes in dates. Because temporal responses differed markedly among species, calendar guilds of plants have changed, which suggests alterations of interspecific relationships in plant communities from Mediterranean ecosystems.
Long‐term transpiration change with rainfall decline in a Mediterranean Quercus ilex forest
Authors: LIMOUSIN J. M. , RAMBAL S. , OURCIVAL J. M. , ROCHETEAU A. , JOFFRE R. , RODRIGUEZ‐CORTINA R. 
Published: January 2009

AbstractIn the Mediterranean basin, precipitation is expected to decline as a consequence of climate change. The response of a Quercus ilex forest in southern France to such a decline in water availability was studied using a 4‐year throughfall exclusion experiment. Seasonal courses of sap flow and leaf water potential were obtained from 2004 to 2007 and used to characterize tree water relations in a control and a dry treatment. The experiment reduced the average precipitation input to the soil by 29%, and resulted in a 23% reduction in annual transpiration. Soil water potential was significantly lower in the dry treatment only during summer drought, but transpiration was reduced all year round even during well‐watered periods. Despite a tight stomatal control over transpiration, whole‐tree hydraulic conductance was found to be lower in the trees growing in the driest conditions. This reduction in water transport capacity was observed jointly with a reduction in leaf transpiring area. Canopy leaf area decreased by 18% in the dry treatment as a consequence of the throughfall exclusion, which was found to validate the ecohydrological equilibrium theory.
Domain analyses of the Runx1 transcription factor responsible for modulating T‐cell receptor‐β/CD4 and interleukin‐4/interferon‐γ expression in CD4+ peripheral T lymphocytes
Authors: Uchino Ryuji 
Published: January 2009

SummaryThe Runx1 transcription factor is one of the master regulators of T‐lymphocyte differentiation. There have been several reports trying to assign a domain within the Runx1 protein that is responsible for gene expression in thymocytes. The Runx1 domains involved in regulating the expression of several genes in peripheral CD4+ T cells were analysed. It was observed that Runx1 over‐expression enhanced the surface expression of CD4 and CD69 molecules via its activation domain and VWRPY domain, and decreased that of T‐cell receptor‐β via its activation domain. Runx1 over‐expression enhanced interferon‐γ expression via its activation and VWRPY domains, and abolished interleukin‐4 expression through its activation domain. Transduction of Runx1 did not down‐regulate CD4 expression until 72 hr of culture, but the repression of CD4 expression became evident after 96 hr. The main region responsible for repressing CD4 expression was the inhibitory domain of Runx1. Taken together, these results lead to a proposal that the regions in Runx1 responsible for modulating gene expression are distinct in thymocytes and in peripheral CD4+ T cells.
Inverse relationship between dendritic cell CCR9 expression and maturation state
Authors: Drakes Maureen L. , Stiff Patrick J. , Blanchard Thomas G. 
Published: January 2009

SummaryCCR9 has been identified on T cells as a chemokine receptor that directs these cells to migrate to the intestine. CCR9 has also been reported on different cell types in the intestine, thymus, liver and peripheral blood. Little is reported concerning the presence of or functional implications of this chemokine receptor on myeloid dendritic cells (DC). In the host, DC encounter a multiplicity of antigenic stimuli to which they mount immune responses. In addition to intracellular and functional changes on sensing antigen, maturation of DC is typically reflected in the up‐regulation of costimulatory molecules on DC. However, alterations in other surface markers may also be an indicator of DC activation. Using bone marrow‐propagated DC these studies investigated cellular maturation in the presence of microbial stimuli and analyzed the relationship of CCR9 expression with DC maturation. Fractionation of DC into CCR9high and CCR9lowsubsets revealed a distinct ability of each subset to induce division in naïve CD4+ T cells. Our results suggest that DC expressing high levels of CCR9 are less activated/mature than DC expressing low levels of CCR9.
Co‐immunization with an optimized plasmid‐encoded immune stimulatory interleukin, high‐mobility group box 1 protein, results in enhanced interferon‐γ secretion by antigen‐specific CD8 T cells
Authors: Muthumani Gowtham , Laddy Dominick J. , Sundaram Senthil G. , Fagone Paolo , Shedlock Devon J. , Kannan Senthil , Wu Ling , Chung Christopher W. , Lankaraman Karthikbabu Mallil , Burns John , Muthumani Karuppiah , Weiner David B. 
Published: January 2009

SummaryDNA vaccination is a novel immunization strategy that has great potential for the development of vaccines and immune therapeutics. This strategy has been highly effective in mice, but is less immunogenic in non‐human primates and in humans. Enhancing DNA vaccine potency remains a challenge. It is likely that antigen‐presenting cells (APCs), and especially dendritic cells (DCs), play a significant role in the presentation of the vaccine antigen to the immune system. A new study reports the synergistic recruitment, expansion and activation of DCs in vivo by high‐mobility group box 1 (HMGB1) protein. Such combinational strategies for delivering vaccine in a single, simple platform will hypothetically bolster the cellular immunity in vivo. Here, we combined plasmid encoding human immunodeficiency virus‐1 (HIV‐1) Gag and Env with an HMGB1 plasmid as a DNA adjuvant in BALB/c mice (by intramuscular immunization via electroporation), and humoral and cellular responses were measured. Co‐administration of this potent immunostimulatory adjuvant strongly enhanced the cellular interferon‐γ (IFN‐γ) and humoral immune response compared with that obtained in mice immunized with vaccine only. Our results show that co‐immunization with HMGB1 can have a strong adjuvant activity, driving strong cellular and humoral immunity that may be an effective immunological adjuvant in DNA vaccination against HIV‐1.
CX3CR1‐deficiency is associated with increased severity of disease in experimental autoimmune uveitis
Authors: Dagkalis Athanasios , Wallace Carol , Hing Benjamin , Liversidge Janet , Crane Isabel J. 
Published: January 2009

SummaryThe role of CX3CR1 in regulating the function of monocytes and microglia was examined in mice in which CX3CR1 had been replaced by green fluorescent protein (GFP). Induction of experimental autoimmune uveitis (EAU) in these mice resulted in increased disease severity at day 23 postimmunization with uveitogenic peptide when compared with CX3CR1‐positive mice and increased apoptosis of neuronal cells in the inner nuclear layer. Resident microglia within the retina were activated equally as EAU developed in mice with or without CX3CR1, as determined by changes in morphology, suggesting that the microglial cell response did not account for the differences. Although the inflammatory infiltrate had increased in mice without CX3CR1 at day 23 postimmunization, the percentage of natural killer cells in the infiltrate was not changed in these mice. Similarly, increased disease severity at this stage was not associated with an overall increased percentage of macrophages in the retinal inflammatory infiltrate or in increased activation of these cells. The increased recruitment of monocytes to the retina in response to EAU induction in CX3CR1GFP/GFP mice compared with CX3CR1GFP/+ mice was not reflected in increased migration away from vessels, leading to marked clustering of GFP+ cells around veins and venules in these mice. It is possible that this monocyte/macrophage clustering leads to the increased severity of disease seen in the mice by focusing and so intensifying the inflammatory response.
Effect of sialic acid loss on dendritic cell maturation
Authors: Crespo Hélio J. , Guadalupe Cabral M. , Teixeira Alexandra V. , Lau Joseph T. Y. , Trindade Hélder , Videira Paula A. 
Published: January 2009

SummarySialic acids are key structural determinants and contribute to the functionality of a number of immune cell receptors. Previously, we demonstrated that differentiation of human dendritic cells (DCs) is accompanied by an increased expression of sialylated cell surface structures, putatively through the activity of the ST3Gal.I and ST6Gal.I sialyltransferases. Furthermore, DC endocytosis was reduced upon removal of the cell surface sialic acid residues by neuraminidase. In the present work, we evaluate the contribution of the sialic acid modifications in DC maturation. We demonstrate that neuraminidase‐treated human DCs have increased expression of major histocompatibility complex (MHC) and costimulatory molecules, increased gene expression of specific cytokines and induce a higher proliferative response of T lymphocytes. Together, the data suggest that clearance of cell surface sialic acids contributes to the development of a T helper type 1 proinflammatory response. This postulate is supported by mouse models, where elevated MHC class II and increased maturation of specific DC subsets were observed in DCs harvested from ST3Gal.I−/− and ST6Gal.I−/− mice. Moreover, important qualitative differences, particularly in the extent of reduced endocytosis and in the peripheral distribution of DC subsets, existed between the ST3Gal.I−/− and ST6Gal.I−/− strains. Together, the data strongly suggest not only a role of cell surface sialic acid modifications in maturation and functionality of DCs, but also that the sialic acid linkages created by different sialyltransferases are functionally distinct. Consequently, with particular relevance to DC‐based therapies, cell surface sialylation, mediated by individual sialyltransferases, can influence the immunogenicity of DCs upon antigen loading.
Granulocyte colony‐stimulating factor‐induced immature myeloid cells inhibit acute graft‐versus‐host disease lethality through an indoleamine dioxygenase‐independent mechanism
Authors: Joo Young‐Don , Lee Sun‐Mi , Lee Soo‐Woong , Lee Won‐Sik , Lee Sang‐Min , Park Ji‐Kyoung , Choi Il‐Whan , Park Sae‐Gwang , Choi Inhak , Seo Su‐Kil 
Published: January 2009

SummaryGranulocyte colony‐stimulating factor (G‐CSF)‐mobilized donor graft tissue used for peripheral blood stem cell transplantation contains a large number of immature myeloid cells that suppress alloreactive donor T cells, resulting in an inhibition of acute graft‐versus‐host disease (GVHD). However, the molecular mechanism underlying the suppressive function of immature myeloid cells is not fully understood. Here, we investigated whether indoleamine 2,3‐dioxygenase (IDO) is related to the suppressive mechanism of G‐CSF‐induced immature myeloid cells (gMCs). We found that Gr‐1+ CD11b+ cells were highly induced in G‐CSF‐injected donor graft tissue, which is a phenotype of immature myeloid cells, resulting in an inhibition of acute GVHD lethality by suppressing alloreactive donor T‐cell expansion. IDO was not detected in primary isolated gMCs; however, this enzyme was markedly induced after treatment with interferon‐γ (IFN‐γ). This level was significantly higher in IFN‐γ‐treated gMCs than in bone marrow myeloid cells, which promote alloreactive T‐cell responses. We next investigated the functional role of IDO in gMC‐mediated inhibition of acute GVHD lethality. We found no changes in gMC‐mediated survival or alloreactive donor T‐cell suppression when IDO activity was blocked using 1‐methyl tryptophan. In addition, there was no difference in gMC‐mediated survival rates between recipients transferred with either wild‐type gMCs or IDO−/− gMCs. Taken together, our data suggest that gMC‐mediated inhibition of lethal acute GVHD is through an IDO‐independent mechanism.
A continuous T‐bet expression is required to silence the interleukin‐4‐producing potential in T helper type 1 cells
Authors: Zhuang Yonghua , Huang Zan , Nishida Jun , Brown Melissa , Zhang Lin , Huang Hua 
Published: January 2009

SummaryTo develop into committed T helper type 1 (Th1) cells, naive CD4+ T cells not only need to acquire the capacity to produce interferon‐γ (IFN‐γ), but they also need to gain the ability to silence their interleukin‐4 (IL‐4) ‐producing potential. How Th1 cells silence their Th2 cytokine‐producing potential is an important yet unresolved issue in Th1 immunity. We found that a lack of IL‐4 stimulation was not sufficient to silence the IL‐4‐producing potential in activated CD4+ T cells and that Th1‐promoting factor was required. Although it has been shown that T‐bet is a crucial factor in suppressing Il4 gene expression, it is unclear whether a continuous presence of T‐bet is required to silence the Il4 gene in Th1 cells. To address this problem, we used an inducible form of T‐bet – a T‐bet‐oestrogen receptor fusion molecule (T‐bet‐ER). We found that the activation of T‐bet during primary or secondary culture was sufficient to silence IL‐4‐producing potential. On the other hand, the inactivation of T‐bet after naïve CD4+ T cells had differentiated into Th1 cells resulted in derepression of Il4 gene transcription. Additionally, we found that T‐bet is required to maintain Ifng expression. Our data demonstrate that the continuous expression of T‐bet is required for Th1 cells to silence their IL‐4‐producing potential.
The immunogenicity of L1210 lymphoma clones correlates with their ability to function as antigen‐presenting cells
Authors: Cycon Kelly A. , Clements James L. , Holtz Renae , Fuji Hiroshi , Murphy Shawn P. 
Published: January 2009

SummaryMajor histocompatibility complex class II (MHCII) antigen expression is directly correlated with immunogenicity, and inversely correlated with tumorigenicity, in clones of the L1210 murine B lymphoma. Moreover, loss of MHCII expression on human diffuse large B‐cell lymphoma is associated with dramatic decreases in patient survival. Thus, the role that MHCII antigens play in the progression of B‐cell lymphomas is clinically important. In this study, we investigated the basis for the immunogenicity of MHCII+ L1210 clones. Immunogenic, but not tumorigenic L1210 clones stimulated the proliferation of naïve T cells and their interleukin (IL)‐2 production, which indicates that the immunogenic clones can function as antigen‐presenting cells (APCs). However, subclonal variants of the immunogenic L1210 clones, which form tumours slowly in mice, could not activate T cells. The costimulatory molecules B7‐1, B7‐2 and CD40 were expressed on the immunogenic L1210 clones, but not the tumorigenic clones. Importantly, the tumour‐forming subclonal variants expressed MHCII and B7‐1, but lacked B7‐2 and CD40. These results suggest that MHCII and B7‐1 expression on L1210 cells is insufficient to activate naïve T cells, and, furthermore, loss of B7‐2 and/or CD40 expression contributes to the decreased immunogenicity of L1210 subclones. Blocking B7‐1 or B7‐2 function on immunogenic L1210 cells reduced their capacity to activate naïve T cells. Furthermore, incubation of immunogenic L1210 cells with CD40 antibodies significantly enhanced APC function. Therefore, the immunogenicity of L1210 cells directly correlates (i) with their ability to stimulate naïve T cells, and (ii) with the concomitant expression of MHCII, B7‐1, B7‐2, and CD40.
The aryl hydrocarbon receptor: a perspective on potential roles in the immune system
Authors: Stevens Emily A. , Mezrich Joshua D. , Bradfield Christopher A. 
Published: January 2009

SummaryThe aryl hydrocarbon receptor (AHR) is a protein best known for its role in mediating toxicity. Over 30 years of research has uncovered additional roles for the AHR in xenobiotic metabolism and normal vascular development. Activation of the AHR has long been known to cause immunotoxicity, including thymic involution. Recent data suggesting a role for the AHR in regulatory T‐cell (Treg) and T‐helper 17 (Th17) cell development have only added to the excitement about this biology. In this review, we will attempt to illustrate what is currently known about AHR biology in the hope that data from fields as diverse as evolutionary biology and pharmacology will help elucidate the mechanism by which AHR modifies immune responses. We also will discuss the complexities of AHR pharmacology and genetics that may influence future studies of AHR in the immune system.
Meta‐analysis of immune epitope data for all Plasmodia: overview and applications for malarial immunobiology and vaccine‐related issues
Authors: VAUGHAN K. , BLYTHE M. , GREENBAUM J. , ZHANG Q. , PETERS B. , DOOLAN D. L. , SETTE A. 
Published: January 2009

SUMMARY We present a comprehensive meta‐analysis of more than 500 references, describing nearly 5000 unique B cell and T cell epitopes derived from the Plasmodium genus, and detailing thousands of immunological assays. This is the first inventory of epitope data related to malaria‐specific immunology, plasmodial pathogenesis, and vaccine performance. The survey included host and pathogen species distribution of epitopes, the number of antibody vs. CD4+ and CD8+ T cell epitopes, the genomic distribution of recognized epitopes, variance among epitopes from different parasite strains, and the characterization of protective epitopes and of epitopes associated with parasite evasion of the host immune response. The results identify knowledge gaps and areas for further investigation. This information has relevance to issues, such as the identification of epitopes and antigens associated with protective immunity, the design and development of candidate malaria vaccines, and characterization of immune response to strain polymorphisms.
Hepatosplenomegaly associated with chronic malaria exposure: evidence for a pro‐inflammatory mechanism exacerbated by schistosomiasis
Authors: WILSON S. , JONES F. M. , MWATHA J. K. , KIMANI G. , BOOTH M. , KARIUKI H. C. , VENNERVALD B. J. , OUMA J. H. , MUCHIRI E. , DUNNE D. W. 
Published: January 2009

SUMMARY In sub‐Saharan Africa, chronic hepatosplenomegaly, with palpable firm/hard organ consistency, is common, particularly among school‐aged children. This morbidity can be caused by long‐term exposure to malaria, or by Schistosoma mansoni, and it is exacerbated when these two occur together. Although immunological mechanisms probably underlie the pathogenic process, these mechanisms have not been identified, nor is it known whether the two parasites augment the same mechanisms or induce unrelated processes that nonetheless have additive or synergistic effects. Kenyan primary schoolchildren, living in a malaria/schistosomiasis co‐transmission area, participated in cross‐sectional parasitological and clinical studies in which circulating immune modulator levels were also measured. Plasma IL‐12p70, sTNF‐RII, IL‐10 and IL‐13 levels correlated with relative exposure to malaria, and with hepatosplenomegaly. Soluble‐TNF‐RII and IL‐10 were higher in children infected with S. mansoni. Hepatosplenomegaly caused by chronic exposure to malaria was clearly associated with increased circulating levels of pro‐inflammatory mediators, with higher levels of regulatory modulators, and with tissue repair cytokines, perhaps being required to control the inflammatory response. The higher levels of regulatory modulators amongst S. mansoni infected children, compared to those without detectable S. mansoni and malarial infections, but exposed to malaria, suggest that S. mansoni infection may augment the underlying inflammatory reaction.
Platinum‐group element signature of the primitive mantle rejuvenated by melt‐rock reactions: evidence from Sumail peridotites (Oman Ophiolite)
Authors: Lorand J.‐P. , Alard O. , Godard M. 
Published: January 2009

AbstractPlatinum‐group element (PGE) abundances in mantle rocks are generally considered to result from a late meteorite addition to the early Earth, post‐dating the core separation event. As such, PGEs are key tracers for the Earth accretion history. For decades, the PGEs systematics of undepleted mantle peridotites has been used to constrain the composition of meteorite impactors involved in the late veneer material. Despite multiple evidence of considerable modifications by partial melting, harzburgites from the Sumail ophiolite (Oman) display a mean PGE composition very akin to recently refined estimates for the Primitive Upper Mantle (PUM) of the Earth. These rocks document a resetting of the PUM signature by percolating basaltic melts, which precipitated Pd‐enriched Cu–Ni sulphides within a strongly Pd‐depleted residual harzburgitic protolith. Such a resetting casts doubt on both the reliability of any PUM estimates and relevance of the PUM concept itself, at least for PGEs.
Extinction, survival and recovery of corals from the Triassic to Middle Jurassic time
Authors: Lathuilière Bernard , Marchal Denis 
Published: January 2009

AbstractRecognizing extinction events and determining their cause at the Triassic/Jurassic (T/J) transition and near the Pliensbachian–Toarcian (Lower Jurassic) boundary is a field of growing interest. We provide arguments for these events through a literature based new evaluation of coral diversity from Triassic to Dogger and a new palaeobiogeographical map. The T/J extinction of corals is clearly related to the breakdown of reef environments. Origination curves show that Hettangian (the lowest Jurassic stage) was not only a survival phase but already rather a recovery phase. Post‐extinction evolution of reefs and their survival only in the northernmost margin of the Tethys support the hothouse hypothesis for the T/J extinction event. During Pliensbachian, many new taxa appear, but mostly solitary corals, not really framebuilders. Many of these taxa do not occur anymore during the following stages. The new increase in diversity is related to the development of Bajocian (Middle Jurassic) reefs.