bluuebunny/crossref_metadata_2025_split huggingface dataset:
Developmental changes in expression patterns of two dopamine receptor genes in mushroom bodies of the honeybee, Apis mellifera
Authors: Kurshan Peri T. , Hamilton Ingrid S. , Mustard Julie A. , Mercer Alison R. 
Published: September 2003

AbstractThe expression patterns of two dopamine receptor genes, Amdop1 and Amdop2, in the developing mushroom bodies of the honeybee brain were determined by using in situ hybridisation. Both genes were expressed throughout pupal development, but their patterns of expression in the three major divisions of mushroom body intrinsic neurons (outer compact cells, noncompact cells, and inner compact cells) were quite distinct. Amdop1 expression could be detected in all three mushroom body cell groups throughout development. Staining for Amdop1 mRNA was particularly intense in newly born Kenyon cells, suggesting that levels of Amdop1 expression are higher in newborn cells than in more mature mushroom body neurons. This was not the case for Amdop2. Amdop2 expression in the mushroom bodies was restricted to inner and outer compact cells during most of pupal development, appearing in noncompact cells only late in metamorphosis or at adult eclosion. In contrast to the case with Amdop1, staining for Amdop2 mRNA was observed in glial cells. Expression of Amdop2 in glial cells was detected only at early stages of glial cell development, when the cells are reported to be actively dividing. This study not only implicates dopamine in the development of honeybee mushroom bodies but also suggests different roles for the two dopamine receptors investigated. J. Comp. Neurol. 466:91–103, 2003. © 2003 Wiley‐Liss, Inc.
Expression pattern of the ether‐a‐gogo‐related (ERG) k+ channel‐encoding genes ERG1, ERG2, and ERG3 in the adult rat central nervous system
Authors: Papa Michele , Boscia Francesca , Canitano Adriana , Castaldo Pasqualina , Sellitti Stefania , Annunziato Lucio , Taglialatela Maurizio 
Published: September 2003

AbstractVoltage‐dependent K+ channels play a pivotal role in controlling cellular excitability within the nervous system. The aim of the present study was to investigate the expression in the adult rat brain of the three ether‐a‐gogo‐related gene (ERG) family members ERG1, ERG2, and ERG3, encoding for K+ channel subunits. To this aim, the distribution of ERG transcripts was studied by means of reverse‐transcription polymerase chain reaction (RT‐PCR) and nonradioactive in situ hybridization histochemistry (NR‐ISH). Furthermore, ERG1 subunit distribution was studied by immunohistochemical analysis. RT‐PCR analysis revealed ERG1, ERG2, and ERG3 expression in the olfactory bulb, cerebral cortex, hippocampus, hypothalamus, and cerebellum. NR‐ISH experiments detected transcripts encoded by all three ERG genes in the cerebral cortex and in all CA subfields and in the granular cell layer of the dentate gyrus of the hippocampus; strong ERG1 signals were also detected in scattered large elements throughout the oriens, pyramidal, and radiatum layers, and in the hilus of the dentate gyrus. In the thalamus, positively labeled neurons were detected in the reticular nucleus with ERG1 and ERG3 and in the anterodorsal nucleus with ERG2 riboprobes. Transcripts for ERG1 and, to a lesser degree, also for ERG3, were detected in the basal ganglia and in several brainstem nuclei. All three ERG genes appeared to be expressed in cerebellar Purkinje cells. Finally, ERG1 expression was also revealed in non‐neuronal elements such as ependymal and subependymal cells along the ventricular walls and hippocampal astrocytes. These results suggest that the K+ channel isoforms of the ERG family appear to be expressed in different central nervous system regions where they might differentially control the firing of neurons engaged in several networks. J. Comp. Neurol. 466:119–135, 2003. © 2003 Wiley‐Liss, Inc.
Structural and neurochemical features of postganglionic sympathetic neurons in the superior mesenteric ganglion of spontaneously hypertensive rats
Authors: Krol Karmen M. , Kawaja Michael D. 
Published: September 2003

AbstractPostganglionic sympathetic neurons, which are exquisitely sensitive to small changes in levels of target‐derived nerve growth factor (NGF), express two transmembrane receptors: 1) the trkA receptor mediates neuron survival and neurite outgrowth; and 2) the p75 neurotrophin receptor (p75NTR) enhances neuronal responsiveness of trkA to NGF. Elevating levels of NGF induces several morphological and neurochemical alterations in sympathetic neurons, including axonal sprouting, increased levels of p75NTR mRNA relative to trkA mRNA, and increased accumulations of NGF in hypertrophied somata. Spontaneously hypertensive rats (SHR) display both elevated NGF levels and increased sympathetic axonal innervation of the mesenteric vasculature. In this investigation we assessed whether sympathetic neurons innervating the mesenteric vasculature of SHR display other features indicative of increased levels of target‐derived NGF. In 5‐week‐old SHR, levels of both p75NTR and trkA mRNA in mesenteric sympathetic neurons were significantly elevated compared to levels in age‐matched control rats. By 15 and 30 weeks of age, levels of p75NTR mRNA expression in mesenteric sympathetic neurons were similar between SHR and control rats. Accumulations of NGF were depleted in the sympathetic somata of 15‐ and 30‐week‐old SHR compared to age‐matched control rats. Moreover, sympathetic neurons in SHR were not hypertrophied, as the sizes of somata were comparable between SHR and control rats. Our data illustrate that despite having augmented levels of NGF in the mesenteric vasculature, SHR do not display many of the morphological and neurochemical features that are associated with an enhanced responsiveness by sympathetic neurons to elevated levels of target‐derived NGF. J. Comp. Neurol. 466:148–160, 2003. © 2003 Wiley‐Liss, Inc.
Inhibition of T helper 2‐type responses, IgE production and eosinophilia by synthetic lipopeptides
Authors: Akdis Cezmi A. , Kussebi Fatimah , Pulendran Bali , Akdis Mübeccel , Lauener Roger P. , Schmidt‐Weber Carsten B. , Klunker Sven , Isitmangil Gülbu , Hansjee Natasha , Wynn Thomas A. , Dillon Stephanie , Erb Peter , Baschang Gerhard , Blaser Kurt , Alkan Sefik S. 
Published: September 2003

AbstractIn allergy and asthma, the fine balance between the T helper (Th) 1, Th2 and T regulatory cytokine responses appears to be shifted towards Th2. Here, we report that synthetic lipopeptides which contain the typical lipid part of the lipoprotein of gram‐negative bacteria stimulate a distinct regulatory cytokine pattern and inhibit several Th2 cell‐related phenomena. The most potent analogue of synthetic lipopeptides, lipopeptide CGP 40774 (LP40) was not active in MyD88‐deficient mice and stimulated Toll‐like receptor (TLR)‐2, but not TLR‐4. LP40 potentiated the production of IFN‐γ and IL‐10, but not IL‐4 and IL‐5 by human T cells. In addition, triggering of TLR‐2 by lipopeptides promoted the in vitro differentiation of naive T cells towards IL‐10‐ and IFN‐γ‐producing T cells and suppressed IL‐4 production by Th2 cells. Accordingly, LP40 inhibited IgE production induced by allergen, anti‐IgD antibody,
Nippostrongylus brasiliensis or murine acquired immunodeficiency virus. Furthermore, ovalbumin‐induced lung eosinophilic inflammation was abolished and Schistosoma mansoni egg‐induced granuloma size and eosinophil counts were suppressed in mice by LP40. These results demonstrate that stimulation of TLR‐2 by lipopeptides represents a novel way for possible treatment of allergy and asthma by regulating the disrupted cytokine balance.
Mannose‐binding lectin engagement with late apoptotic and necrotic cells
Authors: Nauta Alma J. , Raaschou‐Jensen Nicoline , Roos Anja , Daha Mohamed R. , Madsen Hans O. , Borrias‐Essers Maria C. , Ryder Lars P. , Koch Claus , Garred Peter 
Published: September 2003

AbstractThe serum opsonin mannose‐binding lectin (MBL) has been shown to be involved in the handling of apoptotic cells. However, at what stage in the process this happens and whether this mediates activation of complement is unknown. Cells rendered apoptotic or necrotic were incubated with purified MBL/MBL‐associated serine protease (MASP) complexes and assessed by flow cytometry and fluorescence microscopy. MBL bound specifically to late apoptotic cells, as well as to apoptotic blebs and to necrotic cells, but not to early apoptotic cells. Binding of MBL could be inhibited by EDTA as well as with an antibody against the CRD region. Addition of C1q, another serum opsonin involved in the handling of apoptotic cells, prior to MBL partly inhibited MBL binding to apoptotic cells and vice versa. MBL/MASP could initiate deposition of purified complement C4 on the target cells. However, addition of MBL/MASP to whole serum deficient for both C1q and MBL did not enhance deposition of C4, but MBL enhanced phagocytosis of apoptotic cells by macrophages. These results demonstrate that MBL interacts with structures exposed on cells rendered late apoptotic or necrotic and facilitates uptake by macrophages. Thus, MBL may promote non‐inflammatory sequestration of dying host cells.
Early granuloma formation after aerosol Mycobacterium tuberculosis infection is regulated by neutrophils via CXCR3‐signaling chemokines
Authors: Seiler Peter , Aichele Peter , Bandermann Silke , Hauser Anja E. , Lu Bao , Gerard Norma P. , Gerard Craig , Ehlers Stefan , Mollenkopf Hans J. , Kaufmann Stefan H. E. 
Published: September 2003

AbstractAmong the first cells to invade a site of infection, polymorphonuclear neutrophils (PMN) play an important role in the control of numerous infections. While PMN are considered critical for control of acute infections, their role in chronic infections remains less well understood. Here we report that PMN are essential for accurate early granuloma formation during chronic M. tuberculosis infection without influencing mycobacterial growth restriction. The PMN‐mediated regulation of granuloma formation depended on chemokines signaling through CXCR3, in particular MIG, as indicated by immune histochemical analysis of lung sections from C57BL/6 wild‐type and CXCR3–/– mutant mice and supported by microarray transcriptome analysis. Hence, PMN play a central role in regulating the focal granulomatous response in the lung, and this early granuloma formation can be segregated from long‐term protection against pulmonary M. tuberculosis infection.
Myeloid marker expression on antiviral CD8+ T cells following an acute virus infection
Authors: Lin Yinling , Roberts Tonya J. , Sriram Venkataraman , Cho Sungyoo , Brutkiewicz Randy R. 
Published: September 2003

AbstractCD11b, CD11c, and F4/80 are normally used to define dendritic cell and/or macrophage populations. In this study, the expression of all three markers was observed on CD8+ T cells following infection of mice with several distinct viruses. Using lymphocytic choriomeningitis virus as a model virus, it was found that relatively more CD11b+CD8+ and CD11c+CD8+ T cells were present in the periphery than in primary lymphoid organs; in contrast, the F4/80+CD8+ T cell population was more prevalent in the spleen. All three myeloid markers were detected on virus‐specific CTL. The expression of CD11b and CD11c on CD8+ T cells correlated with their level of CTL activity, whereas the F4/80+CD8+ T cell population increased after the peak of the CTL response but did not have higher CTL activity. These data suggest that there is a differential induction of CD11b, CD11c, and F4/80 on virus‐specific CD8+ T cells following an acute virus infection.
Pivotal roles of the parasite PGD2 synthase and of the host D prostanoid receptor 1 in schistosome immune evasion
Authors: Hervé Maxime , Angeli Véronique , Pinzar Elena , Wintjens René , Faveeuw Christelle , Narumiya Shuh , Capron André , Urade Yoshihiro , Capron Monique , Riveau Gilles , Trottein François 
Published: September 2003

AbstractProstaglandins (PG) are important modulators of immune and inflammatory responses. We recently demonstrated that the production of PGD2 by the helminthic parasite Schistosoma mansoni inhibits the migration of epidermal Langerhans cells (LC) to the draining lymph nodes (DLN). Here, we identify the responsible parasite enzyme as being a 28‐kDa glutathione‐S‐transferase (termed Sm28GST). Intradermal injection of Sm28GST in wild‐type (WT), but not in D prostanoid receptor (DP) 1‐deficient mice abrogates the departure of LC from the epidermis after TNF‐α or FITC treatment. During infection, DP1 deficiency restores LC migration, but does not enhance the rate of T cell proliferation in the skin DLN. However, relative to WT mice, DLN cells from DP1‐deficient infected mice produce dramatically less IFN‐γ and IL‐10, but equal amount of IL‐4. Interestingly, infected DP1‐deficient mice develop a more Th2‐biased humoral immune response, a significantly reduced parasitemia and a decreased egg‐induced inflammatory response in the liver and intestines. Taken together, we propose that DP1 activation by the Sm28GST‐derived PGD2 could represent a strategy for the schistosome to evade host immune defenses. We also suggest that DP1 is important in the Th1/Th2 balance of the immune response and in inflammatory reactions during infection.
Differences in maintenance of CD8+ and CD4+ bacteria‐specific effector‐memory T cell populations
Authors: Schiemann Matthias , Busch Verena , Linkemann Kathrin , Huster Katharina M. , Busch Dirk H. 
Published: September 2003

AbstractOur knowledge about the kinetics and dynamics of complex pathogen‐specific CD8+ T cell responses and the in vivo development of CD8+ memory T cells has increased substantially over the past years; in comparison, relatively little is known about the CD4+ T cell compartment. We monitored and directly compared the phenotypical changes of pathogen (Listeria monocytogenes)‐specific CD8+ and CD4+ T cell responses under conditions leading to effective and long‐lasting protective immunity. We found that the general kinetics of bacteria‐specific CD8+ and CD4+ T cells during the effector and post‐effector phases are synchronized. However, later during the memory phase, CD8+ and CD4+ T cell populations differ substantially. Whereas CD8+ memory T cell populations with immediate effector function are readily detectable in lymphoid and non‐lymphoid tissues and remain remarkablystable in size, antigen‐specific CD4+ effector‐memory T cells decline continuously in frequency over time. These findings have important implications for the better understanding of the in vivo development of protective immunity towards intracellular pathogens.
Regulation of PD‐1, PD‐L1, and PD‐L2 expression during normal and autoimmune responses
Authors: Liang Spencer C. , Latchman Yvette E. , Buhlmann Janet E. , Tomczak Michal F. , Horwitz Bruce H. , Freeman Gordon J. , Sharpe Arlene H. 
Published: September 2003

AbstractNewer members of the B7‐CD28 superfamily include the receptor PD‐1 and its two ligands, PD‐L1 and PD‐L2. Here, we characterize the expression of PD‐1, PD‐L1, and PD‐L2 in tissues of naive miceand in target organs from two models of autoimmunity, the pancreas from non‐obese diabetic (NOD) mice and brain from mice with experimental autoimmune encephalomyelitis (EAE). In naive mice, proteiexpression of PD‐1, PD‐L1, and PD‐L2 was detected in the thymus, while PD‐1 and PD‐L1 were detected in the spleen. PD‐L1, but not PD‐L2, was also detected at low levels on cardiac endothelium, pancreatic islets, and syncyciotrophoblasts in the placenta. In pre‐diabetic NOD mice, PD‐1 and PD‐L1 were expressed on infiltrating cells in the pancreatic islets. Furthermore, PD‐L1 was markedly up‐regulated on islet cells. In brains from mice with EAE, PD‐1, PD‐L1, and PD‐L2 were expressed on infiltrating inflammatory cells, and PD‐L1 was up‐regulated on endothelium within EAE brain. The distinct expression patterns of PD‐L1 and PD‐L2 led us to compare their transcriptional regulation in STAT4–/–, STAT6–/–, or NF‐κB p50–/–p65+/– dendritic cells (DC).PD‐L2, but not PD‐L1, expression was dramatically reduced in p50–/–p65+/– DC. Thus, PD‐L1 and PD‐L2 exhibit distinct expression patterns and are differentially regulated on the transcriptional level.
Death of peripheral CD8+ T cells in the absence of MHC class I is Fas‐dependent and not blocked by Bcl‐xL
Authors: Markiewicz Mary A. , Brown Ian , Gajewski Thomas F. 
Published: September 2003

AbstractProductive immune responses require an appropriate environment to support peripheral CD8+ T cell survival. Although host MHC class I molecules appear to be required for this process, the cellular and molecular requirements have not been comprehensively studied. Using adoptive transfer of 2C/recombinase‐activating gene‐2 (RAG‐2)–/– TCR‐transgenic T cells, we found that the survival of both naive and effector CD8+ T cells was dependent upon host expression of the same MHC class I alleles that supported thymic selection. Expression of appropriate MHC class Iby either bone marrow‐ or non‐bone‐marrow‐derived cells was sufficient, suggesting that professional antigen‐presenting cells were not mandatory. In contrast to MHC class I, neither T cell expression of CD28 nor host expression of ICAM‐1 was required for peripheral T cell survival. Finally, T cell death in the absence of appropriate host MHC class I was overcome by elimination of Fas signaling but not by overexpression of Bcl‐xL by CD8+ T cells. These results suggest that, in the absence of a survival signal provided by engagement of host MHC/self peptide complexes, CD8+ T cells die via a Fas‐dependent, mitochondria‐independent pathway.
T cell development and function in CrkL‐deficient mice
Authors: Peterson Amy C. , Marks Reinhard E. , Fields Patrick E. , Imamoto Akira , Gajewski Thomas F. 
Published: September 2003

AbstractThe adapter protein CrkL has been implicated in multiple signal transduction pathways in hematopoietic cells. In T lymphocytes, the recruitment of CrkL‐C3G complexes has been correlated with hyporesponsiveness, implicating CrkL as a potential negative regulator. To test this hypothesis we examined T cell activation in CrkL‐deficient mice. The CrkL–/– genotype was partially embryonic lethal. In viable CrkL–/– mice, peripheral blood counts were normal. The thymus from CrkL–/– mice had 40% fewer cells compared to littermates, but the proportion of thymocyte subsets was comparable. There was no discernable alteration in T cell function as reflected by T cell numbers, expression of memory markers, IL‐2 production, proliferation, and differentiation into Th1/Th2 phenotypes. Immunization induced comparable levels of IgG2a and IgG1 antibodies. Chimeric mice, generated by transfer of CrkL–/– fetal liver cells into irradiated RAG2–/– recipients, also showed normal T cell function, arguing against selection via partial embryonic lethality. Our results indicate that CrkL is not absolutely required for T cell development or function, and argue against it being an essential component of a negative regulatory pathway in TCR signaling.
CCR6 has a non‐redundant role in the development of inflammatory bowel disease
Authors: Varona Rosa , Cadenas Vanesa , Flores Juana , Martínez‐A. Carlos , Márquez Gabriel 
Published: September 2003

AbstractAntigen‐loaded tissues such as the intestinal mucosa must simultaneously elicit appropriate immune response to innocuous bacteria and food proteins, and to potentially harmful antigens. Impairment of the mechanisms controlling this response may mediate the excessive immune reaction that can lead to tissue destruction and inflammatory intestinal diseases, including inflammatory bowel disease. The intestinal epithelium influences local immune responses through the expression of adhesion molecules, costimulatory factors, cytokines and chemokines. CCL20, a β‐chemokine expressed in epithelia from colon and other intestinal tissue, plays a role in immune responses of intestinal mucosa, as deduced from the defects in intestinal leukocyte homeostasis shown by mice lacking CCR6, the CCL20 receptor. We studied the response of CCR6‐deficient mice in two models of inflammatory bowel disease. The data show that absence of CCR6 resulted in less severe intestinal pathology in animals treated with dextran sodium sulfate. Conversely, CCR6 deficiency alters leukocyte homeostasis and the cytokine environment in the intestinal mucosa; these changes are sufficient to confer susceptibility to trinitrobenzene sulfonic acid‐induced intestinal inflammation in the otherwise resistant C57BL/6J mouse strain. These results suggest that the CCR6/CCL20 axis has a critical, non‐redundant role in the in vivo control of immune responses in the intestine.
Production of the soluble pattern recognition receptor PTX3 by myeloid, but not plasmacytoid, dendritic cells
Authors: Doni Andrea , Peri Giuseppe , Chieppa Marcello , Allavena Paola , Pasqualini Fabio , Vago Luca , Romani Luigina , Garlanda Cecilia , Mantovani Alberto 
Published: September 2003

AbstractPTX3 is a prototypic of long pentraxin consisting of an N‐terminal portion coupled to a C‐terminal pentraxin domain, the latter related to short pentraxins (C‐reactive protein and serum amyloid P component). PTX3 is a soluble pattern recognition receptor, which plays a non‐redundant role in resistance against selected pathogens and in female fertility. The present study was designed to analyze the production of PTX3 by human dendritic cells (DC) and to define the role of different innate immunity receptors in its induction. Human monocyte‐derived DC produced copious amounts of PTX3in response to microbial ligands engaging different members of the Toll‐like receptor (TLR) family (TLR1 through TLR6), whereas engagement of the mannose receptor had no substantial effect. DC werebetter producers of PTX3 than monocytes and macrophages. Freshly isolated peripheral blood myeloid DC produced PTX3 in response to diverse microbial stimuli. In contrast, plasmacytoid DC exposed to influenza virus or to CpG oligodeoxynucleotides engaging TLR9, did not produce PTX3. PTX3‐expressing DC were present in inflammatory lymph nodes from HIV‐infected patients. These results suggest that DC of myelomonocytic origin are a major source of PTX3, a molecule which facilitates pathogen recognition and subsequent activation of innate and adaptive immunity.
Correction: Sphingosine 1 phosphate induces the chemotaxis of human natural killer cells. Role for heterotrimeric G proteins and phosphoinositide 3 kinase
Authors: Kveberg L. , Bryceson Y. , Inngjerdingen M. , Rolstad B. , Maghazachi A. 
Published: September 2003

AbstractVol. 32(7) 2002, pp 1856‐1864A mistake has been discovered in the Materials and methods and legends to Figs. 5 and 6, which indicate that the anti‐PI3Kγ is made in rabbit, whereas anti‐PI3Kβ is made in goat.Thus, the correct versions are rabbit anti‐PI3Kβ (S‐19) and goat anti‐PI3Kγ (N16).
Inductively coupled plasma emission spectrometric determination of minerals in catfish frame
Authors: Losso Jack N. , Munene Cate N. , Moody Michael W. 
Published: September 2003

AbstractThe concentration of 14 major and trace elements in catfish (Ictalurus punctatus) frames was determined and analyzed for differences. Three frames were obtained each week for five consecutive weeks in the spring and the fall of 2000. The frames were freed of remaining flesh, dried, treated by microwave dissolution technique and the minerals determined by inductively coupled plasma optical emission spectrometry (ICP‐OES). The mean calcium concentration (mg/kg, dry basis) in the spring (140 400) was not significantly (P > 0.05) different from that in fall (167 000). Among the heavy metals (Cd, Pb, and Al) the concentration of Cd varied significantly (P < 0.05) from week to week but not from season to season. The concentration of all the above‐mentioned heavy metals did not exceed the critical level for human consumption.