bluuebunny/crossref_metadata_2025_split huggingface dataset:
Retracted: Transactivation of CCL20 gene by Epstein–Barr virus latent membrane protein 1
Authors: Okudaira Taeko , Yamamoto Kazuo , Kawakami Hirochika , Uchihara Jun‐Nosuke , Tomita Mariko , Masuda Masato , Matsuda Takehiro , Sairenji Takeshi , Iha Hidekatsu , Jeang Kuan‐Teh , Matsuyama Toshifumi , Takasu Nobuyuki , Mori Naoki 
Published: November 2005

SummaryCCL20 is expected to play a crucial role in the initiation of immune responses and tumour growth. However, expression of CCL20 in Epstein–Barr virus (EBV)‐associated diseases has not been studied. We examined the contribution of EBV infection and EBV‐encoded latent membrane protein (LMP)‐1 to CCL20 expression. EBV infection and LMP‐1 induced CCL20 mRNA expression in the EBV‐negative Burkitt lymphoma (BL) cell lines and the embryonic kidney cell line. Histone deacetylase inhibitor‐stimulated endogenous LMP‐1 also induced CCL20 expression in an EBV‐positive BL cell line. Analysis of the CCL20 promoter showed that it was activated by LMP‐1 C‐terminal activation region (CTAR)‐1 and CTAR‐2. Co‐expression of IκBα, IκBβ, IκB kinase (IKK)α, IKKβ, IKKγ, nuclear factor (NF)‐κB‐inducing kinase and tumour necrosis factor receptor‐associated factor 2 dominant‐negative constructs with LMP‐1 inhibited the activation of the CCL20 promoter by LMP‐1, suggesting that LMP‐1 induces CCL20 via NF‐κB signalling. The requirement for the NF‐κB‐binding site in the CCL20 promoter in LMP‐1 responsiveness was established. Our results indicate that activation of the NF‐κB pathway by LMP‐1 is required for the activation of CCL20 expression.
Inhibition of the phosphatidylinositol‐3 kinase/Akt promotes G1 cell cycle arrest and apoptosis in Hodgkin lymphoma
Authors: Georgakis Georgios V. , Li Yang , Rassidakis Georgios Z. , Medeiros L. Jeffrey , Mills Gordon B. , Younes Anas 
Published: November 2005

SummaryActivation of the phosphatidylinositol 3‐kinase (PI3K) pathway has been linked with tumour cell growth, survival and resistance to therapy in several cancer types. The active, phosphorylated form of Akt (pAkt) was found to be aberrantly expressed in Hodgkin lymphoma (HL)‐derived cell lines and in Hodgkin–Reed–Sternberg (HRS) cells in 27 of 42 (64·3%) of primary lymph node sections of HL, indicative of PI3K activity. Akt phosphorylation was not associated with loss of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) expression, but with its phosphorylation in HL‐cell lines, suggesting that its biological function is impaired. Akt phosphorylation was further induced by CD30 ligand (CD30L), CD40L and receptor activator of nuclear factor kappa B (RANK) ligand. The PI3K inhibitor LY294002 demonstrated antiproliferative effects in a dose‐ and time‐dependent manner, which was associated with Akt dephosphorylation on Thr308 and Ser473 sites and dephosphorylation of the downstream ribosomal protein S6. LY209002 induced cell cycle arrest in the G0/G1 phase and apoptosis, which were associated with upregulation of MDM2, downregulation of cyclin D1, activation of caspase 9 and poly‐ADP‐ribose polymerase cleavage. The Akt inhibitor QLT394 also demonstrated antiproliferative effects in a dose‐ and time‐dependent manner, dephosphorylated ribosomal S6 and cleaved caspase 9. Collectively, these data suggest that the aberrant activation of the PI3K/Akt survival pathway in HRS cells is not because of loss of PTEN expression. Our data suggest that PTEN phosphorylation and activation of CD30, CD40 and RANK may play a role in activating Akt in HRS cells.
Bi‐directional soil/atmosphere N2O exchange over two mown grassland systems with contrasting management practices
Authors: FLECHARD CHRISTOPHE R. , NEFTEL ALBRECHT , JOCHER MARKUS , AMMANN CHRISTOF , FUHRER JÜRG 
Published: November 2005

AbstractNitrous oxide (N2O) fluxes from soil under mown grassland were monitored using static chambers over three growing seasons in intensively and extensively managed systems in Central Switzerland. Emissions were largest following the application of mineral (NH4NO3) fertilizer, but there were also substantial emissions following cattle slurry application, after grass cuts and during the thawing of frozen soil. Continuous flux sampling, using automatic chambers, showed marked diurnal patterns in N2O fluxes during emission peaks, with highest values in the afternoon. Net uptake fluxes of N2O and subambient N2O concentrations in soil open pore space were frequently measured on both fields. Flux integration over 2.5 years yields a cumulated emission of +4.7 kgN2O‐N ha−1 for the intensively managed field, equivalent to an average emission factor of 1.1%, and a small net sink activity of −0.4 kg N2O‐N ha−1 for the unfertilized system. The data suggest the existence of a consumption mechanism for N2O in dry, areated soil conditions, which cannot be explained by conventional anaerobic denitrification. The effect of fertilization on greenhouse gas budgets of grassland at the ecosystem level is discussed.
Interleukin‐16 inhibits interleukin‐13 production by allergen‐stimulated blood mononuclear cells
Authors: El Bassam Souad , Pinsonneault Stéphane , Kornfeld Hardy , Ren Fucheng , Menezes José , Laberge Sophie 
Published: November 2005

SummaryExpression of interleukin (IL)‐16 is increased in bronchial mucosal biopsies of atopic asthmatics compared to normal controls. The functional significance of increased expression of IL‐16 at sites of allergic inflammation is not yet clear. We have previously shown that IL‐16 inhibits IL‐5 secretion by allergen‐stimulated peripheral blood mononuclear cells (PBMC). We investigated whether IL‐16 inhibits the production of other T helper 2 cytokines, namely IL‐13 and IL‐4, by allergen‐specific T cells. PBMC from ragweed‐sensitive atopic subjects were stimulated with allergen extract for cytokine production in the presence or absence of rhIL‐16. Production of cytokines was assessed by enzyme‐linked immunosorbent assay and reverse transcription–polymerase chain reaction. To evaluate whether the modulatory effect of IL‐16 on cytokine synthesis was mediated by interferon‐γ (IFN‐γ), IL‐10, IL‐12 or IL‐18, allergen‐stimulated PBMC were cultured in presence of IL‐16 and neutralizing concentrations of relevant antibodies. Allergen‐stimulated PBMC produced significantly elevated levels of IL‐13 (90–740 pg/ml) as compared to unstimulated PBMC (0–375 pg/ml, P < 0·01). Addition of rhIL‐16 resulted in down‐regulation of IL‐13 mRNA expression as well as significantly reduced amounts of IL‐13 released by allergen‐stimulated PBMC (0–457 pg/ml, P < 0·001), as observed for IL‐5. No effect of IL‐16 was observed on IL‐4 mRNA expression. Treatment with IL‐16 resulted in increased levels of IL‐10 and IL‐18 in allergen‐stimulated cell culture. Neutralization of IFN‐γ, IL‐12, IL‐10 or IL‐18 did not alter the inhibitory effects of IL‐16 on IL‐13 and IL‐5 secretion by allergen‐stimulated PBMC. IL‐16 did not modify IL‐13 synthesis by anti‐CD3‐stimulated CD4+ T cells, but it significantly reduced the production of IL‐5. These data suggest that IL‐16 may play an important immunoregulatory role in allergic states in response to allergen.
The delivery of an antigen from the endocytic compartment into the cytosol for cross‐presentation is restricted to early immature dendritic cells
Authors: Hotta Chie , Fujimaki Haruka , Yoshinari Masahiro , Nakazawa Masatoshi , Minami Mutsuhiko 
Published: November 2005

SummaryDendritic cells (DCs) are the only antigen‐presenting cell population having a cross‐presentation capacity. For cross‐presentation, however, the intracellular antigen‐processing pathway and its regulatory mechanism have not been defined. Here we report the differences in cross‐presentation ability among murine bone marrow‐derived immature DC, early immature day8‐DC and late immature day10‐DC, and fully mature day10 + lipopolysaccharide DC. Day8‐DCs and day10‐DCs show an immature phenotypic profile but are different in morphology. Day8‐DCs can internalize an abundant volume of exogenous soluble ovalbumin (OVA) and result in cross‐presentation. In contrast, day10‐DCs are not able to cross‐present, although they maintain efficient macropinocytosis. Exogenously internalized OVA antigens are stored in the endocytic compartments. The endocytic compartments are temporarily maintained at mildly acidic pH in day8‐DCs and are rapidly acidified in day10‐DCs after uptake of antigens. We show that OVA antigens accumulated in the endocytic compartments move into the cytosol in day8‐DCs but do not in day10‐DCs. NH4Cl‐treatment, which neutralizes the acidic endocytic compartments and/or delays endosomal maturation, restores day10‐DCs for transport the stored OVA antigens from the endocytic compartments into the cytosol. Diphenyleneiodonium chloride‐treatment, which acidifies the endocytic compartments, decreases an amount of transported OVA antigen into the cytosol in day8‐DCs. These data indicate that only the early immature stage of DC interferes with endosomal maturation, even after uptake of exogenous antigens, and then transports the antigens into the cytosol.
OX40 interactions in gastrointestinal nematode infection
Authors: Ierna Michelle X. , Scales Hannah E. , Schwarz Herbert , Bunce Campbell , McIlgorm Anne , Garside Paul , Lawrence Catherine E. 
Published: November 2005

SummaryThe immune expulsion of gastrointestinal nematode parasites is usually associated with T helper type 2 (Th2) responses, but the effector mechanisms directly responsible for parasite loss have not been elucidated. The intestinal inflammatory response accompanying infection with gastrointestinal helminths is thought to be a contributory factor leading to the expulsion of the parasite. However, we have shown that the intestinal inflammation, which is controlled by interleukin (IL)‐4, is not required for parasite expulsion. OX40–OX40 ligand (L) signals have been shown to be important for the development of Th2 immune responses but are also involved in a number of inflammatory diseases including those of the intestine. Here, we have investigated the effect of OX40 and OX40L fusion protein treatment on the induction of protective Th2 responses and enteropathy following infection with the gastrointestinal nematode Trichinella spiralis. Treatment with an OX40–immunoglobulin (Ig) blocking fusion protein resulted in enhanced expulsion of the parasite and an increase in the accompanying mastocytosis, despite unaltered levels of Th2 cytokines. Furthermore, there was a delay in the villus atrophy and crypt hyperplasia usually associated with this infection. In contrast, levels of Th2 cytokines were greatly up‐regulated in mice treated with an OX40L–Ig activating fusion protein, yet the expulsion of the parasite and the enteropathy were unaffected. Therefore, OX40 ligation potentiates the Th2 response without enhancing host protective immune responses, whereas blocking the OX40–OX40L interaction enhances host protection without promoting Th2 cytokine responses during Trichinella spiralis infection.
Rapid and preferential distribution of blood‐borne αCD3εAb to the liver is followed by local stimulation of T cells and natural killer T cells
Authors: Wingender Gerhard , Schumak Beatrix , Schurich Anna , Gessner J. Engelbert , Endl Elmar , Limmer Andreas , Knolle Percy A. 
Published: November 2005

SummaryDissemination of soluble molecules or antigens via the blood stream is considered to lead to a uniform distribution in the various organs of the body, but organ‐specific microarchitecture and vascularization may influence this. Following intravenous injection of αCD3ε antibody (αCD3εAb) we observed clear differences in antibody binding to Fcγ receptor (FcγR)+ antigen‐presenting cells (APCs) or T lymphocytes in different organs. Significant binding of blood‐borne αCD3εAb was only detected in the spleen and liver and not in the thymus or lymph node. In the spleen, only 10% of dendritic cells/macrophages and 40% of T‐cell receptor (TCR)‐β+ cells were positive for αCD3εAb, and, dependent on FcγR‐mediated cross‐linking of αCD3εAb, a similar percentage of splenic TCR‐β+ cells were stimulated and became CD69+. Stimulation of TCR‐β+ cells in the liver was at least as efficient as in the spleen, but almost all T cells and all scavenger liver sinusoidal endothelial cells bound αCD3εAb. In contrast to CD69 up‐regulation, only CD4+ natural killer T (NKT) cells and CD11ahigh CD8+ T cells were activated by αCD3εAb and expressed interferon (IFN)‐γ. Again, IFN‐γ release from NKT/T cells was at least as efficient in the liver as in the spleen. Taken together, our results support the notion that the combination of extensive hepatic vascularization and very high scavenger activity allows the liver to fulfill its metabolic tasks and to promote stimulation of the large but widely distributed hepatic population of NKT/T cells.
Reasons why DBA/2 mice are resistant to malarial infection: expansion of CD3int B220+ γδ T cells with double‐negative CD4– CD8– phenotype in the liver
Authors: Bakir Hanaa Y. , Tomiyama‐Miyaji Chikako , Watanabe Hisami , Nagura Toru , Kawamura Toshihiko , Sekikawa Hiroho , Abo Toru 
Published: November 2005

SummaryDBA/2 (H‐2d) mice are known to be more resistant than C57BL/6 (B6, H‐2b) mice to the non‐lethal 17XNL strain of Plasmodium yoelii. This is a very strange phenomenon because the functions of conventional T cells, especially CD8+ T cells, are known to be somewhat lower in DBA/2 mice than in other strains of mice. We examined herein how immune responses differed between DBA/2 mice and B6 mice during malarial infection. DBA/2 mice and (DBA/2 × B6)F1 (BDF1, H‐2b/d) mice were found to have milder parasitaemia and to recover more quickly from malarial infection than B6 mice. These DBA/2 and BDF1 mice were also found to experience a marked expansion of interleukin (IL)‐2Rβ+ CD3int cells and γδ T cells in the liver, especially in the recovery phase. The expansion of unconventional T cells (i.e. B220+ T cells) was also marked in DBA/2 and BDF1 mice. The majority of B220+ T cells were γδ T cells and these T cells were double‐negative CD4− CD8−. More importantly, the production of immunoglobulin M (IgM)‐type anti‐DNA autoantibody was also higher in DBA/2 and BDF1 mice than in B6 mice. In conjunction with data on cytokine production, these results indicate that primitive T and B cells, namely autoreactive extrathymic T cells and autoantibody‐producing B cells, may be much more activated in DBA/2 mice and therefore resistant to the non‐lethal 17XNL strain of P. yoelii.
Differential regulation of neutrophil chemotaxis to IL‐8 and fMLP by GM‐CSF: lack of direct effect of oestradiol
Authors: Shen Li , Smith Jennifer M. , Shen Zheng , Hussey Stephen B. , Wira Charles R. , Fanger Michael W. 
Published: November 2005

SummaryNeutrophils are a normal constituent of the female reproductive tract and their numbers increase in the late secretory phase of the menstrual cycle prior to menses. Several cytokines are produced in female reproductive tract tissue. In particular granulocyte–macrophage colony‐stimulating factor (GM‐CSF), a potent activator of neutrophils, is secreted in high concentrations by female reproductive tract epithelia. We previously observed that GM‐CSF synergizes strongly with interleukin‐8 (IL‐8) in enhancing chemotaxis of neutrophils. Thus we investigated whether pretreatment of neutrophils with GM‐CSF would prime subsequent chemotaxis to IL‐8 in the absence of GM‐CSF. Surprisingly, a 3‐hr pulse of GM‐CSF severely diminished chemotaxis to IL‐8, whereas N‐formyl‐methyl‐leucyl‐phenylalanine (fMLP)‐mediated chemotaxis was retained. Conversely, when cells were incubated without GM‐CSF they retained IL‐8‐mediated migration but lost fMLP chemotaxis. These changes in chemotaxis did not correlate with expression of CXCR1, CXCR2 or formyl peptide receptor. However, IL‐8‐mediated phosphorylation of p44/42 mitogen‐activated protein kinase was greatly reduced in neutrophils that no longer migrated to IL‐8, and was diminished in cells that no longer migrated to fMLP. Oestradiol, which is reported by some to exert an anti‐inflammatory effect on neutrophils, did not change the effects of GM‐CSF. These data suggest that neutrophil function may be altered by cytokines such as GM‐CSF through modulation of signalling and independently of surface receptor expression.
High‐risk human papilloma virus infection decreases the frequency of dendritic Langerhans' cells in the human female genital tract
Authors: Jimenez‐Flores Rafael , Mendez‐Cruz Rene , Ojeda‐Ortiz Jorge , Muñoz‐Molina Rebeca , Balderas‐Carrillo Oscar , De La Luz Diaz‐Soberanes Maria , Lebecque Serge , Saeland Sem , Daneri‐Navarro Adrian , Garcia‐Carranca Alejandro , Ullrich Stephen E. , Flores‐Romo Leopoldo 
Published: November 2005

SummaryDendritic cells (DC) are often arranged in planar layers in tissues with high antigenic exposure, such as skin and mucosae. Providing an en face view, this arrangement optimizes in situ analysis regarding morphology (even of individual dendrites), topographic distribution (regular/clustered) and quantification. The few reports on human genital DC usually utilize single markers and conventional sections, restricting immunolabelling only to cell parts sectioned by the cut. To better assess DC in situ, we labelled epithelial sheets, prepared from fresh cervix biopsies, with antibodies to major histocompatibility complex (MHC)‐CII, CD1a and Langerin, revealing (with each of these markers) a dense DC network in a planar‐like, regular distribution. Using the hybrid capture system to detect the high‐risk mucotropic human papilloma virus (HPV) group, 16 positive and five negative women were studied and the results were compared between these groups. DC frequency per area was substantially reduced (to ≈ 50% for the three markers) in samples from all HPV‐infected patients compared with samples from controls. Unlike HPV– samples, Langerin+ DC in HPV+ cervix exhibited a highly accentuated dendritic appearance. We believe this to be the first study using these three DC‐restricted markers (Langerin, CD1a and MHC‐CII) in cervical epithelial sheets from high‐risk HPV+ donors and also the first study to demonstrate the morphological and quantitative changes triggered by high‐risk HPV infection. Cervical DC reduction in early, premalignant high‐risk HPV infection might represent viral subversion strategies interfering with efficient antigen handling by the immune system's peripheral sentinels, the DC, perhaps hampering appropriate recruitment and subsequent development of effector (cytotoxic) T cells.
Avifaunal gradients in two arid zones of central Iran in relation to vegetation, climate, and topography
Authors: Kaboli Mohammad , Guillaumet Alban , Prodon Roger 
Published: November 2005

AbstractAim  To identify the ecological factors (related to vegetation, altitude, climate, or geomorphology) that could explain the main gradients of avifaunal richness and composition in arid environments of Central Iran.Location  The study was carried out in two nearby semi‐arid protected areas of the Ispahan province: the Kolah‐Ghazi National Park (c. 50,000 ha; 1540–2535 m a.s.l.) and the Mouteh Wildlife Refuge (c. 220,000 ha; 1493–2900 m a.s.l.). Annual average precipitation and temperature range from 155–205 mm and 15–19.5 °C, respectively. Vegetation cover is sparse.Methods  The two study areas were sampled with a 1 × 1 km grid design. A subset of 405 squares was randomly chosen and each was visited once during spring or summer by a team of five observers walking from one side of a square to the other and back, recording the birds encountered. Raptors and species considered to be accidental or migrating were not taken into account. We first looked for avifaunal, vegetation, and geomorphological gradients using Correspondence Analysis. As we found spatial autocorrelation within our response variables (avifaunal richness, abundance and/or composition), we first calculated an autocorrelation term, then added this autocorrelation term in anova, ancova (separate slope design) and stepwise regression to assess the relative role of spatial autocorrelation and environmental explanatory variables (vegetation, altitude, climate, or topography). We also partitioned the variance of the avifaunal matrix between several sets of co‐variables, after controlling for spatial effects, using a series of partial Canonical Correspondence Analyses.Results  A main gradient, common to the two areas, distinguishes bird species characteristic of flat sedimentary areas and species dwelling in mountainous and/or rocky areas. Despite the generally low values of the correlations measured, we found that richness, abundance and composition of the avifauna were better correlated with topography, especially the altitudinal amplitude within each square, than any other variable, including vegetation. Altitudinal amplitude is related to substrate complexity.Main conclusions  In arid zones of central Iran, topographic features seem to be the main factors structuring avifaunal composition and abundance. Avifaunal composition and richness are mainly correlated with the complexity of the substrate, but both avifaunal richness and abundance increase with altitude, probably in response to decreasing aridity. We did not observe any bird altitudinal zonation in a strict sense. These results contrast with those generally observed in mid‐latitude regions of the Palaearctic.