bluuebunny/crossref_metadata_2025_split huggingface dataset:
Monomer-dimer equilibria of interleukin-8 and neutrophil-activating peptide 2. Evidence for IL-8 binding as a dimer and oligomer to IL-8 receptor B
Authors: Schnitzel Wolfgang , Monschein Ulrike , Besemer Jürgen 
Published: January 2018

Abstract
By chemical cross-linking experiments we show that at physiologically relevant concentrations IL-8 and NAP-2 monomers are in an equilibrium with dimers and even oligomers (Kd 300–800 nM). Oligomerization seems to be more prevalent for IL-8 than for NAP-2. The form in which IL-8 and NAP-2 bind to their specific receptors was analyzed in binding experiments with COS-1 cells expressing IL-8 receptor A or B in recombinant forms. Both receptors were cloned from the human myeloid leukemic cell line AML-193. Type A receptor had high affinity for IL-8 (K d 4 nM) and low affinity for NAP-2 (K d ≥700 nM), whereas the type B receptor was of equally high affinity (K d 2 nM) for both IL-8 and NAP-2. However, IL-8 receptor B could bind specifically three to four times more IL-8 than NAP-2, and NAP-2 was a weak competitor for IL-8 binding to the same receptor. In addition, IL-8, but not NAP-2, could be cross-linked to dimers when bound to IL-8 receptor B. We suggest from these findings that IL-8, but not NAP-2, binds as a dimer and oligomer to IL-8 receptor B. J. Leukoc. Biol. 55: 763-770; 1994.
Role of Fcγ receptors in cancer and infectious disease
Authors: Wallace Paul K , Howell Alexandra L , Fanger Michael W 
Published: January 2018

Abstract
Receptors for the Fc domain of immunoglobulin G (FcγR) provide an interface between specific humoral immunity and the cellular branch of the immune system through their interaction with antibody. Gross-linking FcγR on myeloid cells triggers such diverse functions as clearance of immune complexes, phagocytosis of opsonized pathogens, secretion of reactive oxygen intermediates, and antibody-dependent cellular cytotoxicity. The FcγR play a major role in the removal of antibody-coated infectious agents and are the exclusive trigger molecules for tumor cell killing by human myeloid cells. Studies of FcγR function have been aided by the use of FcγR specific monoclonal antibodies, self-directed target cells, and bispecific antibodies that link target cells or pathogens to specific host cell molecules, including FcγR. These reagents have contributed significantly to our understanding of the role of the different classes of FcγR in mediating protection from various infectious agents and in mediating tumor cell killing. Taken together, these approaches have provided insight into the utility of manipulating Fc?R function in the therapy of cancer and infectious disease. J. Leukoc. Biol. 55: 816–826; 1994.
LPS-inducible nuclear factor in human monocytes that binds the negative regulatory element of the HIV LTR
Authors: Musso Tiziana , Bosco Maria Carla , Longo Dan L , Espinoza-Delgado Igor , Sica Antonio , Cox George W , Gusella G Luca , Forni Guido , Varesio Luigi 
Published: January 2018

Abstract
We studied the constitutive and lipopolysaccharide (LPS)-induced expression of nuclear protein binding to the negative regulatory element (NRE) of the human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR) in fresh human monocytes. We demonstrated the existence of a constitutive factor binding to the NRE 73-bp HpaII/HpaII fragment (–216 to –143) whose expression is up-regulated by LPS treatment. Competition experiments with overlapping oligonucleotides covering the HpaII/HpaII fragment and with mutated oligonucleotides mapped the binding within the TTTCATCAC region (–171 to –163). This binding pattern is unique to human monocytes. J. Leukoc. Biol. 56: 21–26; 1994.
Urokinase-type plasminogen activator enhances invasion of human T cells (Jurkat) into a fibrin matrix
Authors: Kramer Michael D , Spring Herbert , Todd Robert F , Vettel Ulrike 
Published: January 2018

Abstract
The receptor for urokinase-type plasminogen activator (uPA-R) localizes uPA to the cell surface. The receptor-bound uPA converts plasminogen to the trypsinlike endopeptidase plasmin. Thus uPA is involved in the initiation of pericellular proteolysis. Pericellular proteolysis is assumed to facilitate the cellular infiltration into surrounding tissue. The uPA-R has recently been identified as a surface antigen of activated human T lymphocytes. We have characterized the uPA-R of the human CD4+ T cell line Jurkat by immunological (flow cytometry), biochemical (ligand blotting), and physico-chemical (Scatchard blotting) methods. The collective data suggest that the human CD4+ T cell line Jurkat expresses a cell surface receptor for uPA similar to that of myelo/monocytes and normal T cells with regard to size, affinity, ligand specificity, and antigenicity. Binding studies using exogenous uPA and subsequent functional assays revealed that receptor-bound uPA retains its enzymatic activity. Saturation of the Jurkat cell uPA-R with exogenous uPA facilitated cellular invasion into fibrin matrices in vitro. uPA-dependent invasion was inhibited in the presence of an anti-catalytic monoclonal anti-uPA antibody. We propose that uPA-R-bound uPA may facilitate the invasiveness of uPA-R-positive T lymphocytes. J. Leukoc. Biol. 56: 110–116; 1994.
Overview of HIV interactions with macrophages and dendritic cells: the other infection in AIDS
Authors: Crowe Suzanne M , Kornbluth Richard S 
Published: January 2018

Abstract
Since AIDS was first recognized as a unique clinical entity, a massive amount of effort has been devoted to the understanding and control of HIV infection. Several early reports indicated that HIV could infect cells of macrophage lineage, and, more recendy, the interactions between HIV and dendritic cells have become clearer. However, these cells have a special biology which has not always been taken into account by HIV researchers, although the virus itself has evolved special variants with the capacity to infect macrophages. Accordingly, the Second International Workshop on HIV and Cells of Macrophage Lineage was held in Sydney, Australia on December 6 and 7, 1993, in conjunction with the joint meeting of the Australasian Society for Immunology and the Society for Leukocyte Biology. The Organizers were Suzanne Crowe, Tony Cunningham, Richard Kornbluth, Monte Meltzer, and John Mills. Largely through the generosity of the Australian government, the Australian National Centre in HIV Virology Research, and the Society for Leukocyte Biology, this workshop brought together many of the investigators actively working in this field (although neither funds nor time allowed the complete meeting of all the investigators interested in this field). This special issue of the Journal of Leukocyte Biology originated with the ideas presented at this Workshop and provides a partial view of where this field has arrived. In addition, five papers on HIV-induced neuropathology have been included in a minisymposium put together independently of the Workshop by Howard Gendelman.
Macrophage-tropic HIV-1 variants: initiators of infection and AIDS pathogenesis?
Authors: Schuitemaker Hanneke 
Published: January 2018

Abstract
The importance of macrophage-tropic HIV-1 variants in AIDS pathogenesis becomes increasingly clear. Macrophage-tropic HIV-1 variants initiate infection, predominate in the asymptomatic phase, and persist throughout infection, even after the emergence of preferential T cell-tropic HIV-1 variants. HIV-1 infection of macrophages may contribute to the overall immune dysfunction observed in AIDS pathogenesis. Here, our knowledge of the biological variability of HIV-1, and specifically macrophage-tropic HIV-1 variants, is reviewed. Moreover, hypotheses about the mechanism of selection for macrophage-tropic variants in transmission, the mechanism by which these variants selectively persist in the asymptomatic phase, and how they may contribute to the general immune dysfunction are presented. J. Leukoc. Biol. 56: 218–224; 1994.
Significance of T cell apoptosis for macrophages in HIV infection
Authors: Kornbluth Richard S 
Published: January 2018

Abstract
Apoptosis is a major form of cell death in HIV infection. This review presents current ideas on the role of apoptosis in the development of AIDS. HIV may cause apoptosis either directly in individual CD4+ T cells through cellular infection and through the release of gp120 envelope protein, or indirectly by initiating systemic disturbances in the immune system. Furthermore, although apoptosis is often assumed to be a biological dead end, linear, unintegrated retroviral DNA survives apoptosis in avian leukosis virus systems. Macrophages avidly phagocytose apoptosing cells, and the viral DNA in apoptotic debris might spontaneously transfect macrophages and lead to the production of new virions. Such a hypothetical accessory infection pathway may explain why anti-HIV cytotoxic cells are unable to clear this virus from the body. Strategies directed against the “recycling” of the retroviral genomes present in apoptotic debris may ultimately have a role in the treatment of HIV infection. J. Leukoc. Biol. 56: 247–256; 1994.
HIV-1 entry and reverse transcription in macrophages
Authors: O’Brien William A 
Published: January 2018

Abstract
Although CD4 is required for efficient virus entry, it is not sufficient for entry of all primary HIV-1 strains. There may be additional virus-cell interactions, possibly involving the V3 region of the extracellular envelope protein, gp120, that occur following conformational changes induced by CD4 binding. This second interaction would precede fusion events and entry of the virus core. Primary HIV-1 strains appear to have a higher virion envelope density and retain gp120 better than HIV-1 strains adapted to growth in T cell lines in culture. These properties may confer a growth advantage in vivo to primary strains on the basis of less well exposed CD4 binding and neutralization domains. HIV-1 entry into both activated and quiescent T cells, as well as macrophages, is efficient for most primary strains, but there are different patterns of reverse transcription. Productive infection of activated T cells is associated with cell proliferation and accumulation of full-length reverse transcripts within 4 to 6 h. In resting, nondividing T cells, reverse transcription is aborted prior to full-length viral DNA formation. A third pattern of reverse transcription is seen in nondividing cultured macrophages with slow kinetics and accumulation of full-length viral DNA between 36 and 48 h. This rate can be increased by adding exogenous nucleotides, but still not to the rate seen in activated T cells. Future antiretroviral therapies may involve interference with cell-specific functions involved in reverse transcription. J. Leukoc. Biol. 56: 273–277; 1994.
HIV Infection of monocyte-derived macrophages in vitro reduces phagocytosis of Candida albicans
Authors: Crowe Suzanne M , Vardaxis Nicholas J , Kent Stephen J , Maerz Anne L , Hewish Marilyn J , McGrath Michael S , Mills John 
Published: January 2018

Abstract
HIV-1 infection of peripheral blood monocyte-derived macrophages (MDMs) is unrelated to the level of CD4 expression on the surface of the cell, is associated with considerable donor variability, causes minimal cytopathology, and results in peak viral antigen production after 2 weeks of infection. Phagocytosis of opsonized Candida albicans by MDMs infected in vitro with several strains of HIV was compared with that of uninfected cells from the same donors; the proportion of MDMs containing the fluorescein isothiocyanate—labeled yeast was determined by flow cytometry and phase contrast microscopy. The intracellular localization of C. albicans was confirmed by confocal microscopy. Using paired MDMs from nine donors, 81% of uninfected and 53% of HIV-infected MDMs phagocytosed C. albicans. In addition, the number of yeast per cell was significantly higher in uninfected MDMs than in HIV-infected cells (mean 6.1 versus 2.5). These findings may partially explain the high incidence of mucocutaneous candidiasis in HIV-infected patients with advanced disease. J. Leukoc. Biol. 56: 318–327; 1994.
Regulation of HIV expression by viral genes and cytokines
Authors: Vicenzi Elisa , Poli Guido 
Published: January 2018

Abstract
The human immunodeficiency virus (HIV) is the causative agent of the acquired immunodeficiency syndrome (AIDS), a leading cause of death among young individuals. As a complex pathogenic retrovirus, HIV is characterized in vitro and in vivo by the ability to establish either a latent or productive infection of CD4+ T lymphocytes and mononuclear phagocytes (MPs). Viral latency and expression are under the control of both viral genes and several host-related factors. Among these latter, several proinflammatory and immunoregulatory cytokines profoundly affect HIV replication in T lymphocytes and MPs in vitro. Because many of these cytokines have been found to be elevated in HIV-infected individuals, it is likely that they act as regulators of viral expression in vivo. Both viral genes and cytokines regulate transcriptional and posttranscriptional steps in HIV replication. Thus, it is likely that common regulatory pathways between these two distinct classes of regulator molecules will be identified in the near future and will provide potential targets for pharmacologic intervention and treatment of HIV disease. J. Leukoc. Biol. 56: 328–334; 1994.
Interferon-γ protects primary monocytes against infection with human immunodeficiency virus type 1
Authors: Fan Sharon X , Turpin Jim A , Aronovitz Jason R , Meltzer Monte S 
Published: January 2018

Abstract
Monocytes treated with 500 IU/ml human recombinant interferon-γ (rIFN-γ) 1 day before and continuously after human immunodeficiency virus (HIV) infection showed no evidence of virus replication 7 days after addition of the viral inoculum. There was no HIV- associated cytopathic effect, no reverse transcriptase (RT) activity or p24 detected in culture fluids, and no HIV RNA or DNA in cell lysates. Furthermore, no evidence of HIV infection was evident in replicate cultures in which all IFN-γ was removed at 7 days and the cells were cultured for an additional 3 weeks without IFN-γ. The 50% inhibitory dose for reduction of maximum RT activity in HIV-infected monocyte cultures was about 1 IU/ml IFN-γ. No increase in HIV replication was evident in monocytes treated with IFN-γ at any concentration (0 to 5000 IU/ml) or at any time (7 days before to 10 days after HIV infection). In side-by-side experiments with identical monocytes and HIV-1 stock, rIFN-γ was 10 to 20 times more effective than rIFN-α2b for induction of antiviral activity. With both interferons, significant antiviral activity was evident with monocytes treated 1 day before, at the time of, or up to 3 days after infection. At 7 to 10 days after infection (a time at which less than 20% of total cells were infected with HIV) addition of even high concentrations of IFN-α or IFN-γ had no effect on virus replication. These data suggest that the principal action of IFN-α and IFN-γ was directed against the fluid-phase virus. Cell-cell spread of infection within the HIV-infected monocyte culture and extent of virus replication in HIV-infected cells were not affected by interferon treatment. J. Leukoc. Biol. 56: 362–368; 1994.
Histochemical demonstration of hydrogen peroxide production by leukocytes in fixed-frozen tissue sections of inflammatory lesions
Authors: Dannenberg Arthur M , Schofield Brian H , Rao Jay B , Dinh Theresa T , Lee Ki , Boulay Marc , Abe Yasuharu , Tsuruta Junji , Steinbeck Marla J 
Published: January 2018

Abstract
The production of H2O2 by cells in cold paraformaldehyde-fixed frozen sections of inflammatory lesions was histochemically demonstrated by incubating them with diaminobenzidine (DAB) for 2 to 6 h. Catalase (150 μg/ml, about 1400 U/ml) inhibited the reaction, indicating that H2O2 was required to produce the chromogenic DAB product. Granulocytes (PMNs and eosinophils) were the main types of cells stained by the DAB reaction. Positive staining of macrophages was less frequent. The H2O2 was produced by metabolic enzymes that were still active after cell death and mild fixation. An atmosphere of 95 to 100% oxygen enhanced the specific DAB reaction, and an atmosphere of 100% nitrogen eliminated it. The DAB histochemical reaction to detect H2O2 requires the presence of peroxidases to produce the colored reaction product. Within our tissue sections, such peroxidases were evidently present in excess, because addition of low concentrations of H2O2 significantly increased the reaction product. Although some of the H2O2 produced by the granulocytes may have been derived from the dismutation of superoxide (O2-), the NADPH oxidase pathway for O2- formation did not seem to be involved: NADPH oxidase, a rather labile enzyme, should not be active after mild fixation, and diphenyleneiodonium (100 μM), an inhibitor of flavine-requiring NADPH oxidase, did not inhibit the reaction. Reactive nitrogen intermediates were also not involved, because NG-monomethyl-l-arginine and NG-nitro-l-arginine methyl ester, inhibitors of nitric oxide synthetase, did not appreciably inhibit the reaction. We conclude that stable, non-flavine-requiring oxidases, possibly cyclooxygenases or lipoxygenases, produced the H2O2 measured histochemically by our DAB reaction. These studies were made on tissue sections of acute dermal inflammatory lesions produced in rabbits by the topical application of 1% sulfur mustard [bis(2-chloroethyl) sulfide] in methylene chloride. Both intact PMNs and disintegrating PMNs in the base of the crust produced H2O2. Despite the production of H2O2 and the presence of peroxidase activity, no tissue damage was seen microscopically near the H2O2- producing cells, which indicates that the tissues are well protected by the antioxidants present in this self-limiting inflammatory reaction. J. Leukoc. Biol. 56: 436–443; 1994.
Essential involvement of interleukin-8 (IL-8) in acute inflammation
Authors: Harada Akihisa , Sekido Nobuaki , Akahoshi Tohru , Wada Takashi , Mukaida Naofumi , Matsushima Kouji 
Published: January 2018

Abstract
Neutrophil infiltration into inflammatory sites is one of the hallmarks of acute inflammation. Locally produced chemotactic factors are presumed to mediate the sequence of events leading to the infiltration at inflammatory sites. Interleukin-8 (IL-8), a novel leukocyte chemotactic activating cytokine (chemokine), is produced by various types of cells upon stimulation with inflammatory stimuli and exerts a variety of functions on leukocytes, particularly, neutrophils in vitro. However, no definitive evidence has been presented on its role in recruiting and activating neutrophils in the lesions of various types of inflammatory reactions. We administered a highly specific neutralizing antibody against IL-8 in several types of acute inflammatory reactions, including lipopolysaccharide (LPS)-induced dermatitis, LPS/IL-1-induced arthritis, lung reperfusion injury, and acute immune complex-type glomerulonephritis. Anti-IL-8 treatment prevented neutrophil-dependent tissue damage as well as neutrophil infiltration in these conditions. These results suggest that IL-8 plays a causative role in acute inflammation by recruiting and activating neutrophils. J. Leukoc. Biol. 56: 559–564; 1994.
Cross-linking of CD18 in human neutrophils induces an increase of intracellular free Ca2+, exocytosis of azurophilic granules, quantitative up-regulation of CD18, shedding of L-selectin, and actin polymerization
Authors: Walzog Barbara , Seifert Roland , Zakrzewicz Andreas , Gaehtgens Peter , Ley Klaus 
Published: January 2018

Abstract
Polymorphonuclear leukocytes (PMNs) exert most of their physiological functions while adherent to surfaces rather than in suspension. PMN adhesion is largely dependent on the function of the β 2 integrins, CDlla,b,c/CD18. We mimicked engagement of β 2 integrins by antibody cross-linking of CD18 on isolated human PMNs using both intact monoclonal antibody and F(ab’)2 fragments. Within seconds of CD18 cross-linking, we observed a significant, transient rise of intracellular free Ca2+ concentration by 200–300 nM, which was largely due to Ca2+ mobilization from intracellular stores. The Ca2+ signal was blocked after pretreatment with phorbol myristate acetate, an activator of protein kinase C, but not with herbimycin A, a potent inhibitor of tyrosine kinases. In addition to the rise of intracellular free Ca2+ concentration, CD18 cross-linking induced exocytosis of azurophilic granules (release of 26% of total PMN elastase), which was significantly inhibited by herbimycin A. Moreover, 2.2-fold up-regulation of CD18 antigen and significant down-regulation of surface expression of the granulocyte adhesion molecule L-selectin were induced. Granulocyte F-actin content as measured by nitrobenzoxadiazole-phallacidin increased significantly 1 min after CD18 cross-linking. By contrast, CD18 crosslinking by soluble antibodies did not induce superoxide production, but PMNs bound to immobilized monoclonal antibodies against CD18 released significant amounts of superoxide. Initial signaling through β 2 integrins does not appear to be mediated by a phospholipase C isoform activated through tyrosine phosphorylation, because the Ca2+ signal was not altered by herbimycin A. However, more complex cellular responses including exocytosis were found to require tyrosine phosphorylation. We show that engagement of β 2 integrins provides an important stimulatory signal to PMNs inducing degranulation, modulation of L-selectin, and cytoskeletal changes. J. Leukoc. Biol. 56: 625–635; 1994.
Antibody-facilitated macrophage killing of Trypanosoma musculi is an extracellular process as studied in several variations Of an in vitro analytical system
Authors: Albright Julia W , Stewart Michael J , Latham Patricia S , Albright Joseph F 
Published: January 2018

Abstract
Antibody-facilitated macrophage (MP) destruction of Trypanosoma musculi involves ingestion and intracellular degradation of the parasites. It is likely, however, as we show here, that death of the trypanosomes is extracellular and it is the corpses that are ingested by MPs. We have utilized both peritoneal MPs and a cloned line (WLG 5) of mouse MPs to analyze the killing of T. musculi. Both types of MP were more effective when activated by interferon-γ (IFN-γ) rather than lipopolysaccharide (LPS). When activated by both, LPS diminished the killing activity stimulated by IFN-γ, perhaps by changing the spectrum of lysins/toxins released by the MPs. Nitric oxide (NO) was found to be toxic for T. musculi and to be responsible, in part, for MP killing of the parasites. Although antibody and complement in concert caused lysis of T musculi, complement was not required for MP killing of the parasites. In the course of this investigation, we developed an in vitro system, involving line 5 MPs and plasma from infected mice containing resident parasites, that should prove satisfactory for detailed analyses of the mechanisms of the antibody-dependent, cell-mediated cure of T. musculi infection. J. Leukoc. Biol. 56: 636–643; 1994.