bluuebunny/crossref_metadata_2025_split huggingface dataset:
Transduction of recombinant human erythropoietin receptor cDNA into daughter progenitors derived from single CD343+ cord blood cells changes the differentiation profile of daughter progenitors
Authors: Lu Li , Li Zhi-Hua , He Jie , Ge Yue , Rice Susan , Broxmeyer Hal E 
Published: January 2018

Abstract
In this study, we tested the capacity to change the differentiation profile of progenitor cells by retroviral-mediated transduction of EpoR cDNA into one of the paired daughter cells derived from single CD343+ CB cells. Our results show that for the non-viral-treated daughter cells, the majority (99.6%) formed the same colony type. However, with cells transduced with viral vectors, 7.1% of the daughter cells transduced with the EpoR cDNA formed either a burst forming unit-erythroid (BFU-E) or a colony-forming unit-granulocyte, macrophage, erythroid, megakaryocyte (CFU-GEMM) colony compared to the other daughter cell transduced with viral supernatant lacking EpoR cDNA, which formed either a colony-forming unit granulocyte-macrophage (CFU-GM) or a high proliferative potential-colony forming cell (HPP-CFC) colony. Expression of the transduced EpoR cDNA was confirmed in individual colonies by RT-PCR analysis. These results substantiate in a more rigorous fashion our previous results that it is possible to change the Epo-responsive differentiation profile of progenitor cells by transduction into these cells of an EpoR cDNA and this change was apparent only in daughter cells derived from single CD343+ kit+ cells transduced with EpoR cDNA.
Suppressed PHA activation of T lymphocytes in simulated microgravity is restored by direct activation of protein kinase C
Authors: Cooper David , Pellis Neal R 
Published: January 2018

Abstract
Utilizing clinostatic rotating wall vessel (RWV) bioreactors that simulate aspects of microgravity, we found phytohemagglutinin (PHA) responsiveness to be almost completely diminished. Activation marker expression was significantly reduced in RWV cultures. Furthermore, cytokine secretion profiles suggested that monocytes are not as adversely affected by simulated microgravity as T cells. Reduced cell-cell and cell-substratum interactions may play a role in the loss of PHA responsiveness because placing peripheral blood mononuclear cells (PBMC) within small collagen beads did partially restore PHA responsiveness. However, activation of purified T cells with cross-linked CD2/CD28 and CD3/CD28 antibody pairs was completely suppressed in the RWV, suggesting a defect in signal transduction. Activation of purified T cells with PMA and ionomycin was unaffected by RWV culture. Furthermore, sub-mitogenic doses of PMA alone but not ionomycin alone restored PHA responsiveness of PBMC in RWV culture. Thus our data indicate that during polyclonal activation the signaling pathways upstream of PKC activation are sensitive to simulated microgravity.
A novel cell surface proliferation-associated marker expressed on T cells and up-regulated on germinal center B cells
Authors: Campbell J D M , Hopkins J , Howie S E M , Oliver R A , Nichani A K , Goel P , Spooner R L , Glass E J 
Published: January 2018

Abstract
In this study we present data on a novel cell surface antigen recognized by monoclonal antibody (mAb) VPM30, originally thought to recognize only bovine and ovine sIg+ B cells from peripheral blood. Here we show that the antigen, molecular mass 28 kDa, is not only found in B cell follicles in frozen sections, but when used on paraffin sections VPM30 specifically stains B cells in the light zone of germinal centers but not in the mantle or dark zones. In addition we show that the antigen is also expressed by 90% of T cells after activation, with kinetics of antigen expression mirroring those of proliferation. By both size and distribution, the antigen appears to be novel, corresponding to no known cluster of differentiation, and will be of great use in the study of ruminant cellular immune responses.
Th1 and Th2 cytokines cooperate to stimulate mannose-receptor-mediated phagocytosis
Authors: Raveh David , Kruskal Benjamin A , Farland Julien , Ezekowitz R Alan B 
Published: January 2018

Abstract
The mannose receptor is a macrophage surface receptor that mediates both endocytosis and phagocytosis. Previous work has demonstrated that the prototypical Th2 cytokine, interleukin-4 (IL-4), increases both cell-surface receptor expression and mannose receptor-mediated endocytosis, whereas the prototypical Th1 cytokine, interferon-γ (IFN-γ), decreases both surface expression and endocytosis. In many aspects of the immune response, Th1 and Th2 cytokines oppose each others’ actions. We demonstrate that IL-4 and IFN-γ alone and together enhance mannose receptor-mediated phagocytosis, despite opposing effects on cell-surface mannose receptor expression and endocytosis. Thus these usually antagonistic cytokines cooperate in increasing mannose receptor phagocytic function. The cooperative effect of these cytokines is not observed for Fc receptor-mediated phagocytosis. The Th2 cytokine IL-13 exerts similar effects to IL-4. Our results suggest that Th1 and Th2 cytokines may act in concert at sites of inflammation to enhance mannose receptor-mediated phagocytosis of microorganisms. J. Leukoc. Biol. 64: 108–113; 1998.
LPS-binding proteins and receptors
Authors: Fenton Matthew J , Golenbock Douglas T 
Published: January 2018

Abstract
Macrophage activation by Gram-negative lipopolysaccharide (LPS) has been extensively studied in an attempt to define the mechanisms that underlie innate immunity against bacterial pathogens. Dysregulation of these same mechanisms contributes to the pathophysiological consequences of bacterial sepsis. The biological actions of LPS are mediated, at least in part, by both LPS-binding proteins and LPS receptors. Several LPS receptors (CD14, the macrophage scavenger receptor, and the β2 integrins), as well as the serum LPS-binding protein LBP, have been cloned and studied in detail. In addition, insights gained through the use of LPS antagonists have led to a better understanding of a molecule believed to function in conjunction with LPS receptors to transduce signals from the membrane to the cytosol. More recently, the use of knockout mice has greatly expanded our knowledge of the biology of LPS receptors and binding proteins. This review will summarize various phenotypes of mice that lack genes encoding CD14, the scavenger receptor, and LBP. These knockout mice have revealed several unexpected features of LPS action in vivo. Together, these animal models may provide a means to develop and evaluate novel therapeutic approaches to the control of endotoxin shock. J. Leukoc. Biol. 64: 25–32; 1998.
Antioxidants attenuate anthralin-induced skin inflammation in BALB/c mice: role of specific proinflammatory cytokines
Authors: Lange Robert W , Germolec Dori R , Foley Julie F , Luster Michael I 
Published: January 2018

Abstract
Anthralin is the most common therapeutic agent among a small number of pro-oxidant, 9-anthrones effective in the topical treatment of psoriasis. However, the usefulness of this drug is diminished by toxic side effects, including skin irritation and inflammation. The activities of anthralin are believed to be mediated by the generation of reactive oxygen intermediates and anthrone radicals produced in the skin. In this study, the dermal inflammatory response to anthralin was determined using a mouse ear swelling test. Maximum ear swelling induced by anthralin coincided with the elevation of cytokine mRNA expression in the skin, including interleukin-6, granulocyte-macrophage colony-stimulating factor, macrophage inflammatory protein-2, and tumor necrosis factor α at 24 h post challenge. The role of free radical generation in ear swelling and cytokine modulation were examined by systemic administration of cell permeable and impermeable antioxidants before anthralin challenge. Superoxide dismutase and α-tocopherol acetate, but not the glutathione precursor N-acetyl cysteine, were effective inhibitors of anthralin-induced ear swelling and cytokine elevation. Maximum inflammatory cell infiltration occurred 72–96 h post anthralin challenge and was also reduced by antioxidants. These data suggest that oxidative stress, generated at the site of anthralin treatment, alters the expression of dermal chemokines and other cytokines resulting in the recruitment of inflammatory cells. Systemic antioxidant administration may provide opportunities for therapeutic intervention against anthralin-associated toxicities. J. Leukoc. Biol. 64: 170–176; 1998.
Effect of trifluoromethyl ketone-based elastase inhibitors on neutrophil function in vitro
Authors: Huang Yu-Ing , Surichamorn Wanida , Cao Guan-Liang , Meng Min , Pou Sovitj , Rosen Gerald M , Salcedo Theodora W , Strimpler Anne , Veale Chris , Bernstein Peter R , Bonuccelli Catherine M 
Published: January 2018

Abstract
Neutrophils release elastase, which is known secondarily to cause tissue damage. However, it is rapidly inactivated by the endogenous α1-proteinase inhibitor (α1Pi). Nevertheless, under pathological conditions, α1Pi is inactivated by oxidants released from neutrophils, resulting in an excess of elastase at the site of inflammation. This elastase/α1Pi imbalance has been implicated as a pathogenic factor in cystic fibrosis, acute respiratory distress syndrome, and emphysema. Elastase inhibitors, which do not interfere with the microbicidal activity of neutrophils and are resistant to neutrophil-released oxidants, would undoubtedly represent an important advance in the management of neutrophil-mediated tissue injury. We report that a new family of elastase inhibitors ICI200355 and ZD0892 was found to be resistant toward superoxide, hypochlorous acid, hydrogen peroxide, hydroxyl radical, and peroxynitrite mediated degradation as well as having no effect on the formation of these oxidants by activated neutrophils. More importantly, we found that these inhibitors did not interfere with the ability of human neutrophils to phagocytose and to kill Staphylococcus aureus. In conclusion, a new potent class of elastase inhibitors, while blocking the effects of neutrophil elastase, was found not to impede various physiological functions of human neutrophils, in particular the ability of these phagocytic cells to phagocytose and kill bacteria. J. Leukoc. Biol. 64: 322–330; 1998.
Expression of functional major histocompatility complex class II molecules on HMC-1 human mast cells
Authors: Dimitriadou Violetta , Mécheri Salaheddine , Koutsilieris Michael , Fraser William , Al-Daccak Reem , Mourad Walid 
Published: January 2018

Abstract
Mast cells hold a key position in the defensive mechanisms against exogenous intruders. In this study, we investigated whether human mast cells express functional major histocompatibility complex (MHC) class II molecules that can transduce endogenous signals and present staphylococcal enterotoxin A (SEA) to T cells. Similar to HMC-1 human mast cell line, umbilical cord blood-derived mast cells express HLA-DR, -DP and -DQ molecules on their surface. MHC class II molecules expressed on HMC-1 cells bind significantly the SEA (a natural MHC class II ligand), and their ligation with specific mAbs or with SEA, leads ultrastructural chages, suggesting their degranulation. Recognition of SEA-bound MHC class II molecules on HMC-1 mast cells by the T cell receptor of K25 cells, an SEA-specific murine T cell hybridoma, triggers significant IL-2 secretion by these T cell hybridomas. Hence, our data point out the expression of functional MHC class II molecules on human mast cells, reinforcing the implication of these cells in the defense mechanisms of acquired immunity. J. Leukoc. Biol. 64: 791–799; 1998.
Different in vivo tolerogenicity of MHC class I peptides
Authors: Fändrich Fred , Zhu Xiaofung , Schröder Jörg , Dresske Bettina , Henne-Bruns Doris , Oswald Hanno , Zavazava Nicholaus 
Published: January 2018

Abstract
The efficacy of MHC class I-derived peptides to induce tolerance was tested in a cardiac transplantation model. Two 25-mer peptides from the polymorphic region of the DA class I molecule (RT1.Aa) were synthesized by F-moc chemistry and injected intrathymically or intraperitoneally into LEW (RT1.1) responder animals. Intrathymic treatment of the recipient animals with peptide 1 (residues 56–80) accompanied by intraperitoneal treatment with peptide 4 (residues 96–120) led to indefinite survival of allogeneic DA cardiac allografts (n = 7; &gt;100 days). The tolerogenicity of both peptides differed according to the site of inoculation, as donor-specific tolerance was only observed after administration of peptide 1 into the thymus and injection of peptide 2 into the abdominal cavity of LEW recipients, but not vice versa. Donor-specific tolerance was confirmed in vivo by grafting of full-thickness skin and in vitro by appropriate proliferation and cytotoxicity assays using donor and third-party rats. Donor-specific tolerance was associated with up-regulation of interleukin-4, transforming growth factor β, and interleukin-10 gene expression within cardiac allografts, thus suggesting intrathymic clonal deletion and external suppression with expansion of T-helper 2-type lymphocytes as the underlying mechanisms of tolerance induction. J. Leukoc. Biol. 65: 16-27; 1999.
Disparities in the respiratory burst between human and rat neutrophils
Authors: Johnson Jeffrey L , Moore Ernest E , Hiester Andrew A , Tamura Douglas Y , Zallen Garret , Silliman Christopher C 
Published: January 2018

Abstract
The importance of reactive oxygen species (ROS) in neutrophil (PMN)-mediated injury to host tissues has been strongly implicated in a number of animal models. Peculiarities of the laboratory rat PMN, including an apparent paucity of superoxide release, prompted us to examine disparities in the respiratory burst between human and rat PMNs. Using isolated PMNs, we examined oxygen consumption, superoxide release, nitrate/nitrite release, and dihydrorhodamine (DHR) oxidation in response to an array of soluble stimuli. Our findings confirm that intact rat PMNs release little superoxide in comparison to human PMNs when primed and activated by soluble stimuli. For example, PMA-activated human PMNs released superoxide at 10.1 ± 2.7 times the rate of rat PMNs (P &lt; 0.01). However, measurements of oxygen consumption, cell-associated oxidant production (by DHR oxidation) and release of superoxide from electroporated cells suggests that rat PMNs generate oxidants at rates equivalent to human PMNs but preferentially release them in an intracellular compartment. Implications for the study of PMN- mediated oxidant injury in animal models are discussed. J. Leukoc. Biol. 65: 211–216; 1999.
Lineage-specific activation of STAT3 by interferon-γ in human neutrophils
Authors: Caldenhoven Eric , Buitenhuis Miranda , van Djk Thamar B , Raaijmakers Jan A M , Lammers Jan-Willem J , Koenderman Leo , de Groot Rolf P 
Published: January 2018

Abstract
Binding of interferon-γ (IFN-γ) to its heterodimeric receptor induces activation of the tyrosine kinases JAK1 and JAK2 followed by tyrosine phosphorylation of STAT1α. Selective activation of STAT1α at the IFN-γ receptor is achieved by specific interaction between a cytosolic tyrosine motif including Y440 in the IFN-γ receptor α-chain and the SH2 domain of STAT1α. We demonstrate that, in addition to STAT1α, STAT3 is also activated by IFN-γ in human neutrophils. The activation of STAT3 was not found in human eosinophils, monocytes, and HL-60 cells, although the STAT3 protein was expressed in these cells. The cell type-specific activation of STAT3 by IFN-γ was also observed in neutrophils that are differentiated in vitro from human CD34+ hematopoietic stem cells. These results indicate that a single cytokine receptor can activate different STAT family members in a cell-specific manner, which might result in cell-specific gene transcription. J. Leukoc. Biol. 65: 391–396; 1999.
Mucosal and systemic candidiasis in IL-8Rh−/− BALB/c mice
Authors: Balish Edward , Wagner R Doug , Vazquez-Torres Andres , Jones-Carson Jessica , Pierson Carey , Warner Thomas 
Published: January 2018

Abstract
Germ-free BALB/c mice, genetically engineered to be deficient for interleukin-8 (IL-8) receptor homolog (IL-8Rh−/−), were more susceptible to gastric candidiasis after oral challenge and to acute systemic candidiasis after intravenous challenge than IL-8Rh+/+ controls. In comparison to IL-8Rh+/+ mice, the IL-8Rh−/− mice had slower influx of polymorphonuclear neutrophils (PMN) into Candida albicans-infected tissues and a lower percentage of PMN in peritoneal exudate cells (PEC) elicited with heat-killed C. albicans. PEC from IL-8Rh−/− mice exhibited less luminol-dependent chemiluminescence in response to C. albicans and did not kill C. albicans hyphae as well as PEC from IL-8Rh+/+ mice. C. albicans-colonized IL-8Rh−/− mice showed no histological evidence of systemic candidiasis. These results suggest a role for the IL-8Rh in murine resistance to gastric and acute systemic candidiasis, but not in resistance to systemic candidiasis of endogenous origin. J. Leukoc. Biol. 66: 144–150; 1999.
Induction of CC chemokines in human peripheral blood mononuclear cells by staphylococcal exotoxins and its prevention by pentoxifylline
Authors: Krakauer Teresa 
Published: January 2018

Abstract
We investigated the inflammatory processes that might be associated with the arthrogenic activity of Staphylococcus aureus, the principal causative agent of bacterial arthritis. Human peripheral blood mononuclear cells (PBMC) were stimulated with the staphylococcal toxic shock syndrome toxin-1 (TSST-1) or enterotoxin B (SEB) and the production of chemokines was examined. Both TSST-1 and SEB induced high levels (ng/mL) of MIP-1α, MIP-1β, and MCP-1. The induction of these chemokines occurred mostly by direct stimulation of PBMC with staphylococcal exotoxins (SE), without requiring the intervention of IL-1 and TNF-α. The production of SE-induced chemokines was blocked partially by anti-DR and anti-CD2 antibodies. Cell separation revealed monocytes as the cell source of these chemokines. However, addition of purified T cells amplified the levels of chemokine produced, suggesting that cognate interaction of SE bound on antigen-presenting cells with T cells also contributes to chemokine production. The activation and recruitment of leukocytes by these chemokines may contribute to the pathophysiology of septic arthritis caused by staphylococci in humans through tissue injury and the recruitment of T lymphocytes, perhaps also initiating autoimmune responses. Pentoxifylline, an anti-inflammatory agent, completely inhibited the production of these chemokines. J. Leukoc. Biol. 66: 158–164; 1999.
Dendritic cells/chimerism/alleviation of chronic allograft rejection
Authors: Murase Noriko , Ichikawa Naoya , Ye Qing , Chun Hyo Jin , Okuda Toyokazu , Demetris Anthony J 
Published: January 2018

Abstract
Chronic rejection (CR) is the major obstacle of long-term successful organ transplantation. Using a recently developed rat model of CR, we found that heart allografts susceptible to development of CR showed an early (&lt;10 days) dramatic disappearance of donor MHC class II+ cells, including ED2+ tissue macrophages, and an influx of recipient ED1+ macrophages intermixed with small numbers of recipient ED2+ and OX62+ cells. In contrast, donor MHC class II+ cells persisted in allografts resistant to CR with a small influx of recipient macrophages. MHC class II+ cells function as potent modulators of the immune system and may mediate both stimulatory and tolerogenic immune reactions after transplantation. Persistence of donor MHC class II+ antigen-presenting cells (APC) in CR-free graft acceptance suggests that transplantation tolerance is an active immune response requiring antigen presentation to the recipient immune system in the proper context by dendritic cells and other APC. J. Leukoc. Biol. 66: 297–300; 1999.
HHV-8 infection and multiple myeloma
Authors: Sjak-Shie N N , Vescio R A , Berenson J R 
Published: January 2018

Abstract
Human herpes virus 8 (HHV-8) also known as Kaposi's sarcoma-associated herpes virus has been strongly implicated in the pathogenesis of Kaposi's sarcoma (KS), primary effusion lymphoma, and multicentric Castleman disease. Recently, this gamma-herpes virus was also found in the nonmalignant bone marrow dendritic cells of the majority of myeloma patients. In addition, HHV-8 is also detectable in the peripheral blood of most myeloma patients. In contrast, this virus is rarely detected in close contacts of myeloma patients or healthy subjects. Furthermore, only about one-third of patients with monoclonal gammopathy of undetermined significance (MGUS) are infected with HHV-8. Sequencing of HHV-8 DNA isolated from myeloma patients shows both interpatient differences and conserved differences unique to myeloma compared to HHV-8 in other malignancies. Consistent expression of both the viral homologs of interferon regulatory factor and interleukin-8 receptor in myeloma suggests a possible role for these transforming viral genes in the pathogenesis of this disease. J. Leukoc. Biol. 66: 357–360; 1999.
The potential application of ribozymes for the treatment of hematological disorders
Authors: James Helen A 
Published: January 2018

Abstract
With the identification and increasing understanding of the genes involved in neoplastic transformation has come the realization that abrogation of these genes' products may lead to cell death or a return to normalcy. The use of ribozymes and their nucleic acid cousins, antisense oligodeoxynucleotides (ODNs), are two such ways of perturbing the disease-related gene expression. This review will look at the development and application of ribozymes to abrogate gene expression, with particular relevance to hematological settings. Some examples of antisense ODNs will also be mentioned where appropriate. J. Leukoc. Biol. 66: 361–368; 1999.
Impact of the -308 TNF promoter polymorphism on the transcriptional regulation of the TNF gene: relevance to disease
Authors: Abraham Lawrence J , Kroeger Karen M 
Published: January 2018

Abstract
A biallelic G (TNF1 allele) to A (TNF2 allele) polymorphism 308 nucleotides upstream from the transcription initiation site in the tumor necrosis factor (TNF) promoter is associated with elevated TNF levels and disease susceptibilities observed in human subjects. The TNF2 allele is strongly associated with the high-TNF-producing autoimmune MHC haplotype HLA-A1, B8, DR3, with elevated serum TNF levels and a more severe outcome in infectious diseases, such as cerebral malaria. A number of groups have set out to determine whether the -308 polymorphism could affect transcription factor binding and hence influence TNF transcription and expression levels. Although some studies have failed to show any functional difference between the two allelic forms, others have shown that the -308 polymorphism effected transcription factor binding to the region encompassing -308, with the region in the TNF2 allele showing altered binding characteristics. The -308 polymorphism also has been found by some groups to be functionally significant in reporter gene assays in Raji B cells, Jurkat T cells, and U937 pre-monocytic cells. Up to fivefold differences can be measured between TNF1 and TNF2 allelic constructs when the TNF 3′UTR is present, indicating a role in the expression of the polymorphism. Although controversial, the majority of the data support a direct role for the TNF2 -308 allele in the elevated TNF levels observed in TNF2 homozygotes and HLA-A1, B8, DR3 individuals. Elevated TNF levels due to the -308 polymorphism may alter the immune response such that it confers susceptibility to certain autoimmune and infectious diseases. J. Leukoc. Biol. 66: 562–566; 1999.