bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of glycyrrhizin, cyclosporin A, and tumor necrosis factor α on infection of U-937 and MRC-5 cells by human cytomegalovirus
Authors: Numazaki Kei , Nagata Nobuo , Sato Toshiya , Chiba Shunzo 
Published: January 2018

Abstract
Reactivation of latent or persistent human cytomegalovirus (HCMV) infection of monocytes or macrophages occurs under immunosuppressive conditions. We investigated the effect of glycyrrhizin (GL), cyclosporin A (CsA), and tumor necrosis factor-α (TNF-α) on the viral DNA synthesis and antigen expression of HCMV in U-937 and MRC-5 cells. Although GL inhibited the viral antigen expression of HCMV in human monocytic cell line U-937 and human embryonic lung cell line MRC-5 in the study, as determined by flow cytometry and immunofluorescence assay, immediate early HCMV DNA was detected by the polymerase chain reaction. CsA or TNF had no inhibitory effect on HCMV in U-937 or MRC-5 cells. The HCMV infection model with U-937 or MRC-5 cells is of use for clarifying not only the mechanism of persistent infection but also the anti-HCMV effect of chemical agents. J. Leukoc. Biol. 55: 24–28; 1994.
The interleukin-4 receptor: signal transduction by a hematopoietin receptor
Authors: Keegan Achsah D , Pierce Jacalyn H 
Published: January 2018

Abstract
Over the last several years, the receptors for numerous cytokines have been molecularly characterized. Analysis of their amino acid sequences shows that some of these receptors bear certain motifs in their extracellular domains that define a family of receptors called the Hematopoietin receptor superfamily [1–3]. Significant advances in characterizing the structure, function, and mechanisms of signal transduction have been made for several members of this family. The purpose of this review is to discuss the recent advances made for one of the family members, the interleukin (IL) 4 receptor. Other receptor systems have recently been reviewed elsewhere [4–7]. The IL-4 receptor consists of, at the minimum, the cloned 140 kDa IL-4-binding chain with the potential for associating with other chains. The IL-4 receptor transduces its signal by activating a tyrosine kinase that phosphorylates cellular substrates, including the receptor itself, and the 170 kDa substrate called 4PS. Phosphorylated 4PS interacts with the SH2 domain of the enzyme PI-3′-kinase and increases its enzymatic activity. These early events in the IL-4 receptor initiated signaling pathway may trigger a series of signals that will ultimately lead to an IL-4 specific biologic outcome. J. Leukoc. Biol. 55: 272–279; 1994.
Diminished tyrosine protein kinase activity in T cells unresponsive to TCR stimulation
Authors: Tsygankov Alexander Y , Kim Ha W , Pratt Joanne C , Spana Carl , Class Kenneth , Gaulton Glen N , Kamoun Malek , Bolen Joseph B 
Published: January 2018

Abstract
Tyrosine phosphorylation is thought to be one of the earliest steps in antigenic activation of T cells. Three nonreceptor tyrosine kinases, p56lck, p60fyn, and ZAP-70, are known to be involved in T cell receptor (TCR) signaling, albeit their functional roles appear to be different. Whereas p60fyn and ZAP-70 are functionally associated with the T cell antigen receptor, p56lck is essential for TCR signaling without being directly coupled to the TCR. We have studied a mutant variant of the Jurkat T cell line (J32–3.2), in which basal activities of p56lck and p60fyn are 2- to 2.5-fold reduced relative to those in its parental line (J32) while basal activity of ZAP-70 remains unchanged, and compared responses of J32–3.2 and J32 to TCR stimulation. We have demonstrated that tyrosine phosphorylation following CD3 cross-linking in J32–3.2 cells was extremely short-lived and thus insufficient for the induction of subsequent physiological responses. This was at least partially due to the diminished tyrosine kinase activity in these cells. A decrease in the activity of src-related kinases was caused primarily by their lower expression, whereas expression of ZAP-70 was unchanged but its response to CD3 crosslinking was diminished, correlating with the deficient tyrosine phosphorylation of the CD3 -chain, recently observed in J32–3.2. These data are consistent with the idea that sir-related kinases phosphorylate the -chain, which in turn recruits ZAP-70 required to sustain the signal. J. Leukoc. Biol. 55: 289–298; 1994.
Coordinate and noncoordinate colony stimulating factor formation by human monocytes
Authors: Hamilton John A 
Published: January 2018

Abstract
The regulation of macrophage colony-stimulating factor (M-CSF) formation by elutriation-purified human monocytes was studied in vitro and compared with that for granulocyte-macrophage CSF (GM-CSF) and granulocyte CSF (G-CSF). The levels of the three CSFs were measured by immunoassay. Lipopolysac-charide (LPS, 100 ng/ml) was able to enhance CSF formation but the levels were significantly influenced by the presence of a cyclooxygenase product(s) in the cultures. In the presence of LPS, both M-CSF and GM-CSF were up-regulated by cyclooxygenase inhibition (indomethacin, 10-5 M), while G-CSF was down-regulated. Exogenous prostaglandin E2 (PGE2, 10-7 M) reversed the actions of indomethacin. In LPS-treated cells, in contrast to the different regulation by endogenous eicosanoid of M-CSF and GM-CSF formation and G-CSF formation, both interleukin-4 (IL-4, 250 pM) and the glucocorticoid dexamethasone (10-7 M) lowered the amounts of all CSFs. When the actions of CSFs were examined for their effects on CSF formation, M-CSF could not stimulate either GM-CSF or G-CSF synthesis, in contrast to literature findings, while GM-CSF enhanced M-CSF formation but not that of G-CSF. These studies indicate that there can be both coordinate and noncoordinate control of CSF expression by human monocytes. J. Leukoc. Biol. 55: 355–361; 1994.
LGL-1: a potential triggering molecule on murine NK cells
Authors: Mason Llewellyn H , Yagita H , Ortaldo John R 
Published: January 2018

Abstract
Natural killer (NK) cells mediate non-major histocompatibility complex-restricted lysis of tumor cells, lymphokine-activated killing (LAK), antibody-dependent cellular cytotoxicity (ADCC), and reverse ADCC (RADCC). LGL-1+ cells identify a major subset (50%) of murine NK cells. Here we demonstrate that monoclonal antibodies (mAbs) to LGL-1 consistently induce interleukin-2-cultured, and Corynebacterium parvum (in vivo)-activated NK cells to induce RADCC. LGL-1 triggering of activated NK cells coincides with enhanced LGL-1 expression. Testing of murine mAbs to epitopes of CD2 only appears to augment RADCC induced by mAb NK-1.1 on fresh NK cells. Immunoprecipitation of the LGL-1 antigen reveals a highly disulfide-linked 40-kDa homodimer subunit that is N-glycosylated. Therefore, LGL-1 may be similar to other recently characterized NK-associated antigens such as NK-1.1, Ly-49, and NKR-PI. We conclude that although LGL-1 is expressed on “resting” NK cells, enhanced surface expression following activation is usually required for it to act as a signaling molecule. J. Leukoc. Biol. 55: 362–370; 1994.
Transforming growth factor β: a matter of life and death
Authors: McCartney-Francis Nancy L , Wahl Sharon M 
Published: January 2018

Abstract
A wide variety of functions, many of which represent opposing activities, have been attributed to TGF-β, a molecule implicated in embryogenesis, development, and immune and inflammatory processes. This paradoxical behavior of promoting or inhibiting cell growth and function, while important in normal physiology and homeostasis, can contribute to or interrupt pathologic sequelae, making TGF-β a particularly intriguing molecule for study. New transgenic mouse models displaying targeted alterations in TGF-β1 expression offer novel and unique opportunities to determine the essential function(s) of TGF-β. J. Leukoc. Biol. 55: 401–409; 1994.
Transient expression of prostaglandin endoperoxide synthase-2 during mouse macrophage activation
Authors: Riese Jutta , Hoff Torsten , Nordhoff Axel , DeWitt David L , Resch Klaus , Kaever Volkhard 
Published: January 2018

Abstract
We investigated regulation of macrophage prostaglandin production during activation by interferonγ (IFN-γ) and lipopolysaccharide (LPS). An in vitro model was established using the mouse macrophagelike cell line RAW 264.7. Cells were cultivated in the presence of IFN-γ and LPS for up to 48 h and changes in the secretion of nitric oxide (NO) and tumor necrosis factor α (TNF-α) were observed as activation markers. Under these conditions a prompt and strong increase in PGE2 production was found in the first 8 h followed by nearly constant generation of PGE2 during the next 40 h. In contrast, the activity of prostaglandin endoperoxide synthase (PGHS), measured as PGE2 production of microsomal protein fractions, was also increased, but reached a clear maximum at 24 h. Recently a second form of PGHS was cloned (PGHS-2) and specific antibodies and mRNA probes for both isoforms are available. PGHS-2 enzyme was expressed maximally after 24 h of activation whereas PGHS-1 was not influenced. In the presence of IFN-γ and LPS, PGHS-2 mRNA expression reached a maximum at 8 h but PGHS-1 mRNA was not induced during the whole time period. These data indicate that changes in PG synthesis following macrophage activation are due to regulation of PGHS-2 expression. J. Leukoc. Biol. 55: 476–482; 1994.
Cloning and expression of the chicken CD18 cDNA
Authors: Bilsland Caroline A G , Springer Timothy A 
Published: January 2018

Abstract
The leukocyte integrins play a critical role in a number of cellular adhesive interactions during the immune response. We describe here the isolation and characterization of the chicken β2 (CD18) subunit, common to the leukocyte integrin family. The deduced 748-amino-acid sequence reveals a transmembrane protein with 65% and 64% identity with its human and murine homo-logues, respectively. The chicken β2 can associate on the cell surface with the human α subunit of LFA-1 and yields a hybrid molecule capable of binding to purified ICAM-1 and ICAM-3. J. Leukoc. Biol. 55: 501–506; 1994.
Differential expression of mast cell growth factor receptor (c-kit) by peritoneal connective tissue-type mast cells and tissue culture-derived mast cells
Authors: Chen Ben , Scheding Stefan , Nakeff Alexander , Ruan Qingyun 
Published: January 2018

Abstract
The peritoneal cavity of the mouse is a major source of connective tissue-type mast cells (CTMCs). Flow cytometric analysis using biotinylated recombinant murine mast cell growth factor (rMuMGF) showed that 1 to 3% of the cells in the peritoneal cavity exhibited MGF receptor (MGFR) (or c-kit). CTMCs were the only cell types expressing MGFR in the peritoneal cavity, and every one of them expressed MGFR. More than half the peritoneal CTMCs retained the potential to proliferate in the presence of recombinant murine interleukin 3 (rMuIL-3), rMuIL-4, and rMuMGF and gave rise to pure, alcian blue-positive “mast cells,” which actively expressed c-kit transcripts and MGFR. Flow cytometric analysis and receptor assay carried out at 4° showed that the number of MGFRs on culture-derived mast cells (CDMCs) was one-third that of peritoneal CTMCs (6 104 vs. 1.8 105 MGFR/cell). At 37°, the total number of membrane MGFRs detected in CDMC was two to three times more than that detected at 4°, indicating that nearly 70% of total MGFR in CDMCs, compared with only 40% in peritoneal CTMCs, existed as “cryptic sites” unable to interact with exogenous ligand at 4°. Thus, diminished expression of MGFR is one of the phenotypic characteristics associated with CDMCs. J. Leukoc. Biol. 55: 596–602; 1994.
The alternative complement pathway promotes IgM antibody-dependent and -independent adherence of Bacteroides to polymorphonuclear leukocytes through CR3 and CR1
Authors: Foreman Kimberly E , Bjornson Ann B 
Published: January 2018

Abstract
Natural immunoglobulin M (IgM) antibodies act synergistically with the alternative complement pathway to promote opsonization and adherence of Bacteroides thetaiotaomicron and Bacteroides fragilis to polymorphonuclear leukocytes (PMNs). This study characterizes the PMN receptors involved in adherence of Bacteroides opsonized by the alternative pathway and determines the effect of natural IgM antibodies on receptor involvement and on the molecular form of C3 deposited on the bacteria. A model system consisting of the six isolated proteins of the alternative pathway with or without supplemental isolated normal IgM was used for opsonization, and results were compared to those obtained with serum. The results demonstrate that the alternative pathway promotes adherence of Bacteroides to PMNs through complement receptors 1 and 3 (CR3), and epitopes in CR3 besides those mediating iC3b binding do not participate. The results also demonstrate that natural IgM antibodies do not influence the character of the ligands or receptors involved in this interaction. J. Leukoc. Biol. 55: 603–611; 1994.
Remodeling of the plasma membrane after stimulation of neutrophils with f-Met-Leu-Phe and dihydrocytochalasin B: identification of membrane subdomains containing NADPH oxidase activity
Authors: Mukherjee Goutam , Quinn Mark T , Linner John G , Jesaitis Algirdas J 
Published: January 2018

Abstract
Superoxide (O2-) production by neutrophils stimulated with chemotactic peptides [e.g., formylmethionylleucyl-phenylalanine (fMLP)] is transient but increases in rate and duration after pretreatment of the cells with dihydrocytochalasin B (dhCB), suggesting a possible role for the plasma membrane and membrane skeleton in the regulation of the O2- generating system. Analysis of plasma membrane isolated from these cells by isopycnic sucrose density gradient sedimentation showed that there were no significant variation in the distribution of plasma membrane markers between control and dhCB-treated cells, whereas a significant redistribution of plasma membrane markers was observed in dhCB + fMLP-treated cells. Instead of sedimenting to 31–35% sucrose, as in the former two groups, plasma membrane markers were broadly distributed over 25–50% sucrose in the dhCB+fMLP-treated cells. In addition, 80% degranulation was achieved in these cells, whereas little granule release (&lt;5%) was observed in control and dhCB-treated cells. Analysis of the gradient fractions for membrane skeletal (actin and fodrin) and NADPH oxidase (cytochrome b and p47-phox) components in dhCB + fMLP-treated cells demonstrated that the distribution of fodrin, actin, cytochrome b, and p47-phox followed the broad distribution of plasma membrane markers, with an overall eightfold increase in membrane-associated actin. Despite the broad redistribution of plasma membrane markers, the distribution of O2- generating activity remained confined to a narrower peak at 50% sucrose. These results demonstrate that a heterogeneous surface membrane of higher density with a differential distribution of proteins and O2- generating activity are created after dhCB + fMLP treatment; however, domain structure is conserved in the new membrane, with only a subfraction of the reorganized plasma membrane containing all of the components necessary for active O2- generation. Our results support a role for plasma membrane lateral organization and participation of the membrane skeleton in the regulation of the O2- generating system. J. Leukoc. Biol. 55: 685–694; 1994.
Involvement of CD11b/CD18 in enhanced neutrophil adhesion by Fcγ receptor stimulation
Authors: Kusunoki Takashi , Tsuruta Satoru , Higashi Hideo , Hosoi Susumu , Hata Daisuke , Sugie Katsuji , Mayumi Mitsufumi , Mikawa Haruki 
Published: January 2018

Abstract
Neutrophils showed a rapid and transient adhesion to immunoglobulin G (IgG)-coated plates compared with their adhesion to bovine serum albumin (BSA)-coated plates: the adhesion reached a peak after 15 min of incubation and then gradually returned to almost the basal state in 60 min. The addition of monomeric IgG or anti-FcγRII monoclonal antibody (mAb) (IV.3) suppressed the increase in adhesion, whereas anti-FcγRIII mAb (3G8) was hardly effective, indicating that the interaction of FcγR, especially FcγRII, with coated IgG is involved in the process. Adhesion was also blocked by cytochalasin B, suggesting that functional actin filament structures are crucial. Protein kinase inhibitors, erbstatin and genistein, inhibited the adhesion in a dose-dependent manner. The adhesion was inhibited by anti-CDllb (Ml/70) and anti-CD18 (MHM23, TS1/18) mAbs. Moreover, neutrophils from a patient with complete leukocyte adhesion deficiency syndrome did not show increased adhesion to IgG-coated plates. The adhesion of neutrophils to fibrinogen- and BSA-coated plates was also increased when FcγR was stimulated in the fluid phase with soluble aggregated IgG, which was also inhibited by anti-CDllb mAb. Stimulation of neutrophil FcγR with soluble aggregated IgG enhanced the expression of CDllb in concert with the enhanced adhesion. These data collectively suggest that stimulation via FcγR evokes a tyrosine kinase-dependent and actin filament-dependent intracellular signal that enhances the specific and nonspecific adhesive activity of neutrophils, presumably through the activation of CDllb/CD18. J. Leukoc. Biol. 55: 735–742; 1994.
Differential effects of cAMP-elevating drugs on stimulus-induced cytosolic calcium changes in human basophils
Authors: Botana Luis M , MacGlashan Donald W 
Published: January 2018

Abstract
Drugs that elevate cAMP levels in human basophils are known to inhibit immunoglobulin E (IgE)-mediated histamine release. We have examined whether cAMP-active agents inhibit the cytosolic Ca2+, [Ca2+]i, response that normally accompanies activation of basophils. As previously described, this [Ca2+]i response is biphasic, one phase dependent on internal sources of calcium and a second later phase dependent on extracellular calcium, as observed in many cell types. Forskolin and rolipram or their combination had no effect on the initial elevation of cytosolic calcium that follows stimulation with anti-IgE antibody. In contrast, the second phase of the IgE-mediated calcium response was inhibited by these agents. For IgE-mediated responses, the relative efficacy of various cAMP active agents (rolipram forskolin &lt; dibutyryl cAMP &lt; forskolin + rolipram) for the inhibition of histamine release and the second-phase calcium response was similar and roughly paralleled the measured increase in basophil cAMP. In contrast, neither the first nor the second phase of the f-Met-Leu-Phe (fMLP)-induced calcium response was inhibited by any of the cAMP-active agents tested. Indeed, at low concentrations of fMLP, a combination of forskolin and rolipram caused slight enhancement of the calcium response. This result was consistent with the observations that these agents had no effect or caused slight enhancement of histamine or leukotriene released induced by fMLP. Similarly, cAMP-active agents caused no inhibition of C5a or phorbol ester (phorbol myristate acetate)-induced histamine release. These observations suggest that inhibition of the phase of the calcium response that is dependent on extracellular calcium could account for the inhibition of histamine release by these agents. However, these studies also suggested that (1) this is effect is not exerted at the level of the inositol trisphosphate (InsP3) receptor or InsP3 metabolism and (2) the mechanisms that maintain the second-phase calcium response are possibly distinct for IgE- and fMLP-mediated reactions because cAMP-active agents inhibited the second-phase response of only one stimulus. J. Leukoc. Biol. 55: 798–804; 1994.
Selective Mycobacterium avium–induced production of nitric oxide by human monocyte-derived macrophages
Authors: Dumarey Claude H , Labrousse Valérie , Rastogi Nalin , Vargaftig B Boris , Bachelet Maria 
Published: January 2018

Abstract
Infection with a virulent strain of Mycobacterium avium, but not with virulent Mycobacterium tuberculosis or avirulent Mycobacterium smegmatis, induced the formation of nitric oxide by human monocyte-derived macrophages. This process was not affected by lipopolysaccharide or cytokines such as interferon-γ or tumor necrosis factor α. M. avium-induced nitric oxide production was significantly decreased by NG-monomethyl-l-arginine, a potent inhibitor of nitric oxide synthase activity, without any significant enhancement of intramacrophagic mycobacterial growth. Infection with all the three mycobacterial species induced a significant activation of phospholipase A2 activity of macrophages as evidenced by the increased release of thromboxane A2. Finally, nitric oxide production by human monocyte-derived macrophages required infection with live M. avium, as neither gamma-irradiated M. avium nor the subcellular fractions of this microorganism (cell wall, cytosol) were able to trigger nitric oxide synthesis. J. Leukoc. Biol. 56: 36–40; 1994.
Human neutrophil respiratory burst response to influenza A virus occurs at an intracellular location
Authors: Kazhdan Misha , White Mitchell R , Tauber Alfred I , Hartshorn Kevan L 
Published: January 2018

Abstract
We have studied in detail the in vitro interactions of influenza A viruses (IAVs) with human neutrophils to clarify why these cells become dysfunctional during IAV infection. Unosponized IAV elicited a respiratory burst response in neutrophils which, like that triggered by formylmethionyl-leucyl-phenylalanine (fMLP), involved mediation of signal-transducing GTP-binding proteins and tyrosine kinase activation. The IAV-induced response differed from that provoked by fMLP in that H2O2 was produced without concomitant O2- release. IAV also did not cause extracellular release of granule enzymes in cytochalasin B-treated neutrophils. Using chemiluminescence assays, the respiratory burst response to IAV was found to occur at an intracellular location. These findings may, in part, explain the anomalous nature of the respiratory burst response elicited by IAV and suggest strategies for determining the mechanism of IAV-induced neutrophil deactivation. J. Leukoc. Biol. 56: 59–64; 1994.
Differentiated U937 cells exhibit increased bactericidal activity upon LPS activation and discriminate between virulent and avirulent Listeria and Brucella species
Authors: Caron Emmanuelle , Liautard Jean-Pierre , Köhler Stephan 
Published: January 2018

Abstract
In the study of interactions between facultative intracellular pathogens and macrophages, monocytic cell lines have the advantages of showing defined states of activation and lacking genetic variation among donors, thus yielding reproducible results. Nonpathogenic Escherichia coli K12 were killed at similar rates in the U937 cell line differentiated into macrophage-like cells by phorbol myristate acetate (PMA) or by the combination of retinoic acid (RA) and vitamin D3 (VD). Complete elimination was reached only when cells were activated by lipopolysaccharide for 30 min prior to infection, and it was further enhanced when bacteria were opsonized by specific immunoglobulin G. Both types of differentiation led to intracellular multiplication of virulent Listeria monocytogenes and to elimination of the animal pathogen Listeria ivanovii. For both strains, conditions for intracellular survival were more favorable in PMA-differentiated U937. During infection, RA/VD-differentiated U937 could discriminate between the human pathogen Brucella suis S1, which strongly multiplied, and the animal pathogen Brucella canis, which survived without multiplication. U937 cells differentiated by RA and VD therefore represent a basic model in bacteria-human macrophage interactions. J. Leukoc. Biol. 56: 174–181; 1994.