bluuebunny/crossref_metadata_2025_split huggingface dataset:
Bactericidal/permeability‐increasing protein promotes complement activation for neutrophil‐mediated phagocytosis on bacterial surface
Authors: Nishimura H. , Gogami A. , Miyagawa Y. , Nanbo A. , Murakami Y. , Baba T. , Nagasawa S. 
Published: March 2003

SummaryThe neutrophil bactericidal/permeability‐increasing protein (BPI) has both bactericidal and lipopolysaccharide‐neutralizing activities. The present study suggests that BPI also plays an important role in phagocytosis of Escherichia coli by neutrophils through promotion of complement activation on the bacterial surface. Flow cytometric analysis indicated that fluorescein‐labelled E. coli treated with BPI were phagocytosed in the presence of serum at two‐ to five‐fold higher levels than phagocytosis of the bacteria without the treatment. In contrast, phagocytosis of the fluoresceined bacteria with or without treatment by BPI did not occur at all in the absence of serum. The phagocytosis stimulated by BPI and serum was dose‐dependent. The effect of BPI on phagocytosis in the presence of serum was not observed on Gram‐positive bacteria (Staphylococcus aureus). Interestingly, the complement C3b/iC3b fragments were deposited onto the bacterial surface also as a function of the BPI concentration under conditions similar to those for phagocytosis. Furthermore, the BPI‐promoted phagocytosis was blocked completely by anti‐C3 F(ab′)2 and partially by anti‐complement receptor (CR) type 1 and/or anti‐CR type 3. These findings suggest that BPI accelerates complement activation to opsonize bacteria with complement‐derived fragments, leading to stimulation of phagocytosis by neutrophils via CR(s).
Generation of cellular immunity to lymphocytic choriomeningitis virus is independent of CD1d1 expression
Authors: Spence Philip M. , Sriram Venkataraman , Van Kaer Luc , Hobbs Jacqueline A. , Brutkiewicz Randy R. 
Published: March 2003

SummaryCD1 molecules are cell surface glycoproteins, structurally similar to major histocompatibility complex (MHC) class I molecules. The murine CD1d1 molecule has been shown to be essential for the positive selection of a unique subpopulation of T cells [the natural killer (NK) T cells], as CD1d1‐deficient mice lack NK T cells. These cells have recently been suggested to play an important role in the induction of innate immunity (i.e. NK cells) and the regulation of immune homeostasis. As such, it was asked whether NK T cells were necessary for the generation of cellular immunity to an acute virus infection. In these studies, the Armstrong strain of lymphocytic choriomeningitis virus (LCMV), a classic inducer of NK cells, and its pathogenic variant clone 13 were used. When NK‐cell activity was assessed on day 3 post‐LCMV infection, surprisingly, it was found that CD1d1‐deficient mice could generate NK‐cell activity at wild‐type levels. Likewise, LCMV‐specific cytotoxic T‐lymphocyte (CTL) activity in CD1d1‐deficient mice was indistinguishable from that generated in wild‐type mice. Additionally, viral titres in the spleen (LCMV Armstrong) and blood (LCMV clone 13) of infected CD1d1‐deficient mice were at comparable levels to those found in wild‐type mice, as were virus infection‐induced increases in cell surface H‐2Kb in the spleen. Therefore, these results suggest that the LCMV‐induced generation of NK‐cell and virus‐specific CTL activity, as well as viral clearance, are independent of CD1d1 expression.
Glycolipid targets of CD1‐mediated T‐cell responses
Authors: Moody D. Branch , Besra Gurdyal S. 
Published: March 2003

SummaryMembers of the CD1 family of antigen‐presenting molecules bind and present a variety of mammalian and microbial glycolipids for specific recognition by T cells. CD1 proteins accomplish their antigen‐presenting function by binding the alkyl chains of the antigens within a deep, hydrophobic groove on the membrane distal surface of CD1, making the hydrophilic elements of the antigen available for contact with the variable regions of antigen‐specific T‐cell receptors. Most models of CD1‐restricted T cells function in infectious, neoplastic, or autoimmune diseases and are based on the premise that CD1‐restricted T‐cell responses are initiated by alterations in cellular glycolipid content. Although a growing number of self, altered self and foreign glycolipid antigens have been identified, the cellular mechanisms that could lead to the generation of antigenic glycolipids within cells, or control the presentation of particular classes of altered self or microbial glycolipids in disease states have only recently come under investigation. Here we review the structures of known glycolipid antigens for T cells and discuss how the chemical nature of these antigens, which is quite different from that of peptides, influences their recognition by T cells.
Genetic fusion of human insulin B‐chain to the B‐subunit of cholera toxin enhances in vitro antigen presentation and induction of bystander suppression in vivo
Authors: Sadeghi Hamid , Bregenholt SØren , Wegmann Dale , Petersen Jacob S. , Holmgren Jan , Lebens Michael 
Published: March 2003

SummaryThe pentameric B‐subunit of cholera toxin (CTB) can be used as an efficient mucosal carrier of either immunogenic or tolerogenic T‐cell epitopes. In this study a series of fusions was constructed between the genes encoding CTB and the B‐chain of human insulin (InsB). The resulting fusion proteins were expressed in Escherichia coli and isolated as cytoplasmic inclusion bodies that were then dissolved and assembled in vitro. GM1 enzyme‐linked immunosorbent assay (ELISA), sodium dodecyl sulphate–polyacrylamide gel electrophoresis (SDS–PAGE) and Western blot analyses showed that the protein construct in which InsB was fused to the C‐terminus of a CTB monomer (CI) assembled into structures that both bound to the receptor GM1 ganglioside and reacted with monoclonal antibodies to CTB and insulin. Fusion of InsB to the N‐terminus of CTB resulted in protein that could not assemble into pentameric CTB. In vitro assays showed that the CI fusion protein was 300‐fold more potent than native insulin at inducing interleukin‐2 (IL‐2) production by an insulin‐specific T‐cell hybridoma. When administered orally, the CI fusion protein induced efficient immunological suppression of ovalbumin‐specific T‐cell responses in mice co‐immunized parenterally with insulin and ovalbumin. These results demonstrate the stability, GM1 receptor‐binding activity and antigenic authenticity of the CI fusion protein as well as its ability to elicit insulin‐specific T‐cell responses in vitro. In addition, we demonstrate that the CI fusion protein induces efficient immunosuppression after oral administration, raising the possibility of using such constructs in the treatment of type‐1 diabetes.
MD41, a novel T helper 0 clone, mediates mast‐cell dependent delayed‐type hypersensitivity in mice
Authors: Torii Ikuko , Morikawa Shigeru , Harada Takayuki 
Published: March 2003

SummaryIn a previous study on mouse, we have shown that delayed‐type hypersensitivity (DTH) could be classified into two types according to MC requirement. The first type of DTH could be elicited by sensitization with methylated human serum albumin (MHSA) in complete Freund's adjuvant (CFA) in both wild type and mast‐cell deficient (W/Wv) mice. The second type could be elicited by MHSA in incomplete Freund's adjuvant (IFA) sensitization in wild type but not W/Wv mice. While the former was related to classic tuberculin (tbc)‐type DTH, the latter appeared to be a novel mast‐cell dependent DTH (MD‐DTH). In order to investigate the mechanism of MD‐DTH, in this study, we generated an effector T‐cell clone (MD41) from lymph node cells of MHSA in IFA‐sensitized mice and analysed its pattern of cytokine production. Our results from cytokine assays show that following antigen stimulation, MD41 cells produce significant amounts of the T helper 1 (Th1) cytokine interferon‐γ (IFN‐γ) as well as the Th2 cytokines interleukin (IL)‐4 and IL‐10. In addition, double staining for IL‐4 and IFN‐γ revealed that MD41 cells produce both Th1‐ and Th2‐type cytokines simultaneously, which suggest that MD41 represents a Th0 clone rather than a mixture of Th1 and Th2 clones. Adoptive transfer of MD41 cells into wild‐type mice resulted in the development of DTH skin reactions similar to those produced by active sensitization, with very similar histological findings. However, DTH skin reactions could not be induced in W/Wv mice unless first reconstituted with normal bone marrow MC (BM‐MC). Therefore, our study suggests that in conjunction with tissue MC, MD41, a less‐polarized MD‐DTH‐derived Th0 clone, is capable of developing murine DTH to the same extent as strongly polarized Th1 cells and mediates MD‐DTH rather than tbc‐type DTH.
Necessity of the stalk region for immunoglobulin E interaction with CD23
Authors: Chen Bing‐Hung , Ma Check , Caven Timothy H. , Chan‐Li Yee , Beavil Andrew , Beavil Rebecca , Gould Hannah , Conrad Daniel H. 
Published: March 2003

SummaryPreviously, a soluble mouse CD23 chimera, composed of an N‐terminal trimeric isoleucine zipper motif (lz) followed by the entire extracellular region (amino acids 48–331) of CD23 (lz‐CD2348−331), was prepared and exhibited strong binding to rodent immunoglobulin E (IgE). In the current study, we report the construction of a similar human chimeric protein (lz‐huCD2345−321), as well as a series of murine chimeric lz‐CD23 mutants with incremental portions of stalk deleted, to further investigate the role of the stalk region in mediating the CD23–IgE interaction. All chimeric proteins were designed such that the predicted heptad structure of the stalk was retained. IgE binding, as determined by the capacity to inhibit 125I‐IgE from binding to FcεRI‐bearing RBL‐2H3 cells, and by surface plasmon‐resonance analysis using an IgE‐coated sensor chip, was unchanged from the original lz chimera and the binding parameters were similar to those of cell‐surface CD23. The minimal murine chimera that retained IgE‐binding activity was lz‐CD23139−331, which still contains 35 amino acids of the stalk region. When the lz motif was linked to CD23 amino acid 157 (or higher), significant IgE‐binding capacity was lost. With human lz‐CD23, as with mouse, deletion of the stalk greatly reduced IgE‐binding ability. In summary, the data support the concept that at least a portion of the stalk region of CD23 plays a crucial role in maintaining high‐affinity/avidity interaction with IgE. The lz‐CD23 constructs represent a possible alternative for both blocking the IgE/FcεRI interaction and inhibiting IgE production by B lymphocytes.
Skewed autoantibody reactivity to the extracellular domain of myelin oligodendrocyte glycoprotein in multiple sclerosis
Authors: Tejada‐Simon Maria V. , Hong Jian , Rivera Victor M. , Zhang Jingwu Z. 
Published: March 2003

SummaryMyelin oligodendrocyte glycoprotein (MOG) is found to induce both autoreactive T‐cell and antibody responses associated with demyelinating pathology and is implicated in the pathogenesis of multiple sclerosis (MS). In this study, we addressed the potential association of anti‐MOG immune responses with MS by examining, comparatively, both the T‐cell and antibody responses to recombinant MOG fragments in MS patients and healthy subjects. T cells recognizing MOG were detected in MS patients as well as in healthy subjects, and their precursor frequency in the blood was not increased in patients with MS. MOG‐reactive T cells isolated from both MS patients and healthy subjects exhibited a similar cytokine profile, producing interleukin (IL)‐4, IL‐10 and tumour necrosis factor (TNF), but not interferon‐γ (IFN‐γ), and recognized predominantly the extracellular (residues 1–60) and the transmembrane/cytoplasmic (residues 154–218) domains of MOG. In contrast, anti‐MOG antibodies derived from MS patients displayed a skewed reactivity pattern, even though the occurrence and titres of serum anti‐MOG antibodies were only slightly elevated in MS patients. MS‐derived autoantibodies were predominantly directed at the 1–60 region of MOG, while naturally occurring anti‐MOG antibodies derived from healthy individuals reacted selectively to the 154–218 domain. These differences were statistically significant. The findings of this study are consistent with the presence of anti‐MOG antibodies within demyelinating lesions of MS and their role in the induction of demyelinating pathology in animal models. The study has important implications in the understanding of the autoimmune processes in MS.
Functional and Vβ repertoire characterization of human CD8+ T‐cell subsets with natural killer cell markers, CD56+ CD57− T cells, CD56+ CD57+ T cells and CD56− CD57+ T cells
Authors: Takayama Eiji , Koike Yuji , Ohkawa Takashi , Majima Takashi , Fukasawa Masashi , Shinomiya Nariyoshi , Yamaguchi Takanori , Konishi Mieno , Hiraide Hoshio , Tadakuma Takushi , Seki Shuhji 
Published: March 2003

SummaryWe investigated the individual CD8+ populations with natural killer (NK) cell markers (NK‐type T cell); CD56 single positive (CD56)‐T cells, CD56/CD57 double positive (DP)‐T cells and CD57 single positive (CD57)‐T cells in the peripheral blood. All NK‐type T‐cell populations expressed CD122 and intermediate levels of T‐cell receptor (TCR; regular CD8+ T cells are CD122− and express high levels of TCR). The number of both DP‐T cells and CD57‐T cells, but not CD56‐T cells, gradually increased with age. All NK‐type T‐cell populations produced larger amounts of interferon‐γ than did regular CD8+ T cells after stimulation with interleukin (IL)‐2, IL‐12 and IL‐15. However, CD56‐T cells and CD57‐T cells but not DP‐T cells showed a potent antitumour cytotoxity to NK‐sensitive K562 cells, whereas only CD56‐T cells showed a potent cytotoxity to NK‐resistant Raji cells. Furthermore, although NK‐type T cells produced large amounts of soluble Fas‐ligands, their cytotoxic activities appeared to be mediated by the perforin/granzyme pathway. The oligoclonal or pauciclonal expansions of certain VβT cells were found in each NK‐type T‐cell population. The non‐variant CDR3 region(s) for the TCRβ chain(s) showed CD57‐T cells and CD56‐T cells to be derived from distinct origins, while the DP‐T cell population consisted of a mixture of the clones seen in both CD56‐T cells and CD57‐T cells. Our results suggest that CD57‐T cells and CD56‐T cells are functionally and ontogenically different populations while DP‐T cells appear to originate from both CD56‐T cells and CD57‐T cells.
Memory T‐cell competition for bone marrow seeding
Authors: Di Rosa Francesca , Santoni Angela 
Published: March 2003

SummaryThe presence in the bone marrow of memory CD8 T cells is well recognized. However, it is still largely unclear how T‐cell migration from the lymphoid periphery to the bone marrow is regulated. In the present report, we show that antigen‐specific CD4 T cells, as well as antigen‐specific CD8 T cells, localize to the bone marrow of immunized mice, and are sustained there over long periods of time. To investigate the rules governing T‐cell migration to the bone marrow, we generated chimeric mice in which the lymphoid periphery contained two genetically or phenotypically distinct groups of T cells, one of which was identical to the host. We then examined whether a distinct type of T cell had an advantage over the others in the colonization of bone marrow. Our results show that whereas ICAM1 and CD18 molecules are both involved in homing to lymph nodes, neither is crucial for T‐cell bone marrow colonization. We also observed that memory‐phenotype CD44high T cells, but not virgin‐type CD44−/low T cells, preferentially home to the bone marrow upon adoptive transfer to normal young mice, but not to thymectomized old recipients where an existing memory T‐cell pool precludes their free access. Thus, T‐cell colonization of the bone marrow uses distinct molecules from those implicated in lymph node homing, and is regulated both by the properties of the T cell and by the competitive efficacy of other T cells inhabiting the same, saturable niche. This implies that the homing potential of an individual lymphocyte is not merely an intrinsic property of the cell, but rather a property of the lymphoid system taken as a whole.
Ambiguity in IT adaptation: making sense of First Class in a social work setting
Authors: Henfridsson Ola 
Published: March 2003

AbstractThis paper explores how people make sense of the ambiguity caused by newly introduced information technology (IT) in organizations. A better understanding of these sense‐making processes might provide some basis for improving the way in which information technology is adapted in organizations. On the basis of an interpretive case study, the paper identifies how certain attention structures facilitated and restricted the meaningful construction of IT in a particular organizational context – social work. In this context, the previous coincidence of IT introductions with increasing administrative workload had considerable implications for the way in which a communications technology (First Class) was adapted. On a general level, it is concluded that making sense of ambiguity is an important ingredient in successful IT adaptation.
Chemical and gamma‐ray mutagenesis of the white gene in Aedes aegypti
Authors: Wendell M. D. , Wilson T. G. , Higgs S. , Black W. C. 
Published: March 2003

AbstractA molecular understanding of an insect gene can be facilitated by analysing the phenotypes of mutants for that gene. Protocols were developed for both chemical and gamma‐ray mutagenesis in Aedes aegypti using the white (w) gene as an assay. Wild‐type adult males were subjected to varying doses of either ethyl methanesulphonate (0.1%, 0.5% or 1%) or gamma rays (1500 R or 3000 R), mated to females homozygous for the recessive w mutation, and progeny screened for the w phenotype, indicating non‐complementation. The expression of newly induced w alleles was either complete or mosaic. Gamma‐ray mutagenesis resulted in high (1.65 or 6.39%, depending on dose) induction of mutant alleles for the w gene, but not for a different gene, red‐eye (0.15%). Gamma‐ray‐induced w alleles did not revert at a reasonable frequency following additional irradiation, suggesting that the high rate of gamma‐ray‐induced w mutagenesis is not due to a transposon insertion event.
Analysis of intraspecies polymorphism in the ribosomal DNA cluster of the cockroach Blattella germanica
Authors: Mukha D. V. , Sidorenko A. P. , Lazebnaya I. V. , Wiegmann B. M. , Schal C. 
Published: March 2003

Abstract HindIII restriction digests of the rDNA repeat unit of the German cockroach, Blattella germanica, reveal significant intraspecies sequence polymorphism. This variability is probably caused by structural differences within the nontranscribed spacer regions (NTS) of the ribosomal repeat unit. HindIII rDNA fragment polymorphisms in three cockroach strains show that individuals from different populations may have different HindIII rDNA patterns, whereas individuals within populations exhibit relatively similar rDNA patterns. We suggest that HindIII restriction fragment polymorphisms within cockroach ribosomal DNA will be a valuable tool for measuring population‐level parameters within and between natural cockroach populations.
Organization, evolution and expression of a multigene family encoding putative members of the odourant binding protein family in the medfly Ceratitis capitata
Authors: Christophides G. K. , Mintzas A. C. , Komitopoulou K. 
Published: March 2003

AbstractA multigene family encoding male specific serum polypeptides (MSSPs) that show significant structural similarity to the family of insect odourant binding proteins, has been characterized in the medfly Ceratitis capitata. This family comprises seven members classified in three subgroups, MSSP‐α, MSSP‐β and MSSP‐γ. The genes of subgroups α and β are clustered in tandem in a 35‐kb genomic region, and present an exceptionally high degree of similarity not only in their coding but also in the surrounding regions, while the genes of the γ subgroup are drastically divergent. Although MSSPs are predominantly expressed in the male fat body, detailed expression studies suggest that individual members of this family are expressed in a distinct sex‐ and tissue‐specific manner.
Patterns of DNA sequence variation in chromosomally recognized taxa of Anopheles gambiae: evidence from rDNA and single‐copy loci
Authors: Mukabayire O. , Caridi J. , Wang X. , Touré Y. T. , Coluzzi M. , Besansky N. J. 
Published: March 2003

AbstractPatterns of DNA sequence variation in the ribosomal DNA (rDNA) second internal transcribed spacer (ITS2) and five unlinked single‐copy nuclear loci were examined for evidence of reproductive isolation among four chromosomally recognized taxa of Anopheles gambiae from West Africa: Savanna, Bamako, Mopti and Forest, as well as sibling species An. arabiensis and An. merus. Included among the single‐copy loci were three sequence‐tagged random amplified polymorphic DNA (RAPD) loci, two of which (R15 and R37) had been reported as discriminating between Mopti and other chromosomal forms. Each of the five single‐copy sequences were highly polymorphic in most samples. However, the R15 and R37 loci had no diagnostic value, and therefore are not recommended as tools in recognition of field‐collected An. gambiae chromosomal forms. Although pairwise comparisons between species generally revealed significant levels of differentiation at all five loci, variation was not partitioned by chromosomal form within An. gambiae at any single‐copy locus examined. The few exceptions to these trends appear related to a location either inside or nearby chromosomal inversions. At the tryptophan oxygenase locus inside inversion 2Rb, variation was structured only by inversion orientation and not by taxonomic designation even between An. gambiae and An. arabiensis, providing the first molecular evidence that the 2Rb inversion was transferred between species by introgressive hybridization. By contrast, the rDNA showed fixed differences between species and a difference diagnostic for Mopti, consistent with effective, if not complete, reproductive isolation. The apparent disagreement between the data from this locus and multiple single‐copy loci within An. gambiae may be explained by the much lower effective population size of rDNA, owing to concerted evolution, which confers increased sensitivity at much shorter divergence times. Taken together with the accompanying reports by della Torre et al. (2001), Favia et al. (2001) and Gentile et al. (2001), our data suggest that neutral molecular markers may not have the sensitivity required to detect isolation between these recently established taxa.
The Drosophila gene Yippee reveals a novel family of putative zinc binding proteins highly conserved among eukaryotes
Authors: Roxström‐Lindquist K. , Faye I. 
Published: March 2003

AbstractAn intracellular Drosophila protein, Yippee, was identified in a yeast interaction trap screen as physically interacting with Hyalophora cecropia Hemolin. The Yippee gene was isolated, structurally characterized, and mapped to the region 12A on the X‐chromosome. Yippee contains a putative zinc‐finger‐like metal binding domain. It is the first characterized member of a conserved gene family of proteins present in diverse eukaryotic organisms, ranging from cellular slime mould to humans. A human cDNA clone was isolated and shown to be 76% identical to Drosophila Yippee. Yippee is ubiquitously expressed in different developmental stages of Drosophila and in different fetal tissues from human. Although the Hemolin–Yippee interaction remains to be further elucidated, the high degree of Yippee sequence conservation between a wide range of species suggests that this protein is of general importance in eukaryotes.