bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evidence for the expression of three different BoLA-class II molecules on the bovine BL-3 cell line: determination of a non-DR non-DQ gene product
Authors: Ababou Assia , Goyeneche Julio , Davis William C , Lévy Daniel 
Published: January 2018

Abstract
Studies were conducted to determine the reactivity of six monoclonal antibodies specific for major histocompatibility complex class II molecules expressed on a bovine B cell line homozygous for BoLA-DR and BoLA-DQ alleles. Direct immunoprecipitation, serial immunodepletion experiments, and two-dimensional gel electrophoresis revealed that these antibodies reacted with three different molecules. Bovine orthologues of HLA-DR were recognized by three monoclonal antibodies—H34A, TH12A, and TH14B. Orthologues of HLA-DQ, were characterized by two other monoclonal antibodies, TH22A and TH81A. A third BoLA class II antigen, neither DR nor DQ was revealed by the last monoclonal antibody H42A. The relation of this molecule to known molecules in humans and other species remains to be established. However, cumulative data suggest that the determinant is expressed on a molecule related to HLA-DP. J. Leukoc. Biol. 56: 182–186; 1994.
Susceptibility of dendritic cells to HIV-1 infection in vitro
Authors: Cameron Paul U , Lowe Melinda G , Crowe Suzanne M , O’Doherty Una , Pope Melissa , Gezelter Stuart , Steinman Ralph M 
Published: January 2018

Abstract
We review recent work on the extent of HIV-1 infection of dendritic cells (DCs) and the consequences of exposure to virus. The reported levels of infection of DCs from blood have varied from “explosive” to “undetectable.” The only study that used sorted DCs demonstrated little if any infectability, which may not be surprising given the very low levels of CD4 on the populations that were studied. HIV-1-pulsed, highly purified DCs function as potent antigen-presenting cells during the mixed leukocyte reaction and responses to superantigens. At the same time that the HIV-1-pulsed DCs stimulate CD4+ T cells in DC-T clusters, the virus is transferred to the responding lymphocytes and a vigorous productive infection of the T cells takes place. This pool of transferable HIV-1 is short lived in cultured human blood DCs and likely reflects the capacity of these cells to internalize and recycle vesicles in the endocytic pathway, as revealed with experiments using 0.1-μm fluorescent latex beads. Current efforts are directed to analyzing the interaction of HIV-1 with several populations of DCs that express higher levels of CD4. These include DCs studied in fresh, uncultured blood, as well as skin, thymus, and tonsil DCs. In each case, entry and reverse transcription of HIV-1 are seen, but again, coculture with T cells is required for a productive infection to take place. We conclude that DCs could play a critical role in the pathogenesis of HIV-1 infection, but that the interaction with CD4+ T cells is a critical variable in analyzing the extent of productive infection and its consequences. J. Leukoc. Biol. 56: 257–265; 1994.
The HIV-1 regulatory protein Nef has a specific function in viral expression in a murine macrophage cell line
Authors: Murphy Kathleen M , Sweet Matthew J , Hume David A 
Published: January 2018

Abstract
Expression of reporter genes under the control of the HIV-1 long terminal repeat (LTR) was up-regulated in the murine macrophage cell line RAW264 by cotransfection of a plasmid coding for the viral regulatory protein Nef. To determine if a discrete section of the LTR was exclusively responsive to Nef, a series of promoters was produced by successive 5′ deletions from the LTR up to the boundary of the enhancer region. These truncated promoters were as active as the full-length sequence in the RAW264 cells, but elimination of the direct repeats and one of the three Sp1 sites reduced promoter activity to minimal levels. Transcription driven by all constructs was equally susceptible to the trans-activating effect of Nef and could be increased further by the addition of a Tat-expressing plasmid to the cotransfection. Open reading frames of nef from NL4-3, from HXB2, which has a premature stop, and a fully functional hybrid of the two under the control of the SRα artificial promoter (SV40 early promoter plus HTLV-I R-U5′) were able to trans-activate the LTR in RAW264 cells to the same degree as HXB3 nef under the control of the cytomegalovirus (CMV) immediate-early promoter. A frameshift mutation of Nef at the XhoI site at position 8475 did not abrogate trans-activation of the LTR in macrophages. To further define the effective trans-activation region of Nef, internal deletions were made. Changes downstream of the XhoI site at amino acid 35 resulted in little or no reduction in trans-activation, whereas a deletion between the CMV promoter of the expression plasmid and the XhoI site largely abolished activity. Nef trans-activation of the LTR may be restricted to macrophages. Parallel cotransfection experiments in COS-1 simian fibroblast-like cells showed repression of reporter expression by Nef. Results suggested that the section of nef responsible for trans-activation of the LTR in macrophages differed slightly from that sufficient for trans-repression in fibroblasts. Translation of the protein from the first translation start site (Met-1) rather than from the second in-frame ATG (Met-20) appears to be necessary for the trans-activating effect of Nef in RAW264 cells. Mutation of the initial ATG to ATA led to loss of trans-activating activity. Expression of Nef also has a cytostatic/cytotoxic effect on RAW264 cells indicated by a reduced rate of establishment of stably transfected clones. The cytostatic effect of Nef was not relieved by internal deletions in the coding sequence. The effect required transcription of one of two regions of the nef gene. These observations suggest that effects of Nef on cell growth and LTR-driven transcription in RAW264 cells are not related. Trans-activation of the HIV-1 LTR in the RAW264 cells by the regulatory protein Nef may be due to a novel protein-promoter interaction. J. Leukoc. Biol. 56: 294–303; 1994.
Intracerebral infusion of TNF-α and IL-6 failed to activate latent SIV infection in the brains of macaques inoculated with macrophage-tropic neuroadapted SIVmac
Authors: Joag Sanjay V , Adams Robert J , Pinson David M , Adany Istvan , Narayan O 
Published: January 2018

Abstract
Lymphocyte-tropic (L-tropic) SIVmac predictably causes immunosuppression and AIDS in rhesus macaques. SIV encephalitis, on the other hand, is caused mainly by macrophage-tropic (M-tropic) SIVmac. We have previously described the derivation of M-tropic, neuroadapted SIVmac from molecularly cloned, L-tropic SIVmac239. In this report we show that inoculation of four macaques with neuroadapted virus resulted in L-tropic SIVmac–related diseases in all four but neurological disease in only two of the four animals. Because cocultivation of infected macrophages with CD4+ lymphocytes results in production of tumor necrosis factor α and interleukin-6, we asked whether infiltration of supernatant fluids containing these cytokines into the brains of macaques infected with neuroadapted virus would enhance the development of neurological disease. These procedures failed to promote productive virus replication in the brain. Thus, although different degrees of immunosuppression and AIDS could be induced predictably with L-tropic virus, induction of neurological disease was not predictable even when animals were inoculated with neuroadapted M-tropic virus and inflammatory cytokines were infiltrated into the brains of these animals. J. Leukoc. Biol. 56: 353–357; 1994.
Influence of acridine tracer dyes on neutrophil function
Authors: Hansell Peter , Berger Elaine , Chambers J David , Arfors Karl-E 
Published: January 2018

Abstract
A study was performed to elucidate the effect of two commonly used fluorescent dyes in in vivo microscopic studies, acridine orange (AO) and acridine red (AR), on the ability of phorbol myristate acetate (PMA)-or formyl peptide (fMLP)-stimulated human neutrophils to adhere to a bovine serum albumin matrix and to generate superoxide anions (SOX). Unlabeled stimulated human neutrophils showed 36 ± 9% (PMA, 10-7 M) and 11 ± 7% (fMLP, 10-7 M) adherence to the matrix. This adhesion was CD18 dependent as evidenced by 98% and 92% reduction, respectively, when the anti-CD18 antibody IB4 was included. A dose-dependent inhibition of stimulated human neutrophil adhesion was evident after 30 min of in vitro dye labeling and the EC50 was approximately 70 μg/ml (AR) and 145 μg/ml (AO). SOX generation by PMA-stimulated neutrophils was unaffected up to 100 μg/ml AR and AO but was reduced by 40–60% at higher doses. Rabbit neutrophils labeled in vivo or in vitro with 100 μg/ml AR exhibited 41% and 61% lower SOX generation, respectively. The study indicates that neutrophil function, in terms of ability to adhere to a BSA matrix using CD11/CD18 integrins and to generate SOX upon stimulation, is reduced depending on the dose and choice of fluorescent dye. Caution should be exercised when using these compounds at high concentrations in studies of PMN function. J. Leukoc. Biol. 56: 464–468; 1994.
Interleukin-4 suppresses inflammatory cytokine gene transcription in porcine macrophages
Authors: Zhou Yaling , Lin Gaofeng , Baarsch Mary Jo , Scamurra Ronald W , Murtaugh Michael P 
Published: January 2018

Abstract
Inflammatory cytokines, including interleukin (IL)-1α, IL-1β, IL-8, and tumor necrosis factor α (TNF-α) are produced by macrophages in response to a variety of pathogenic stimuli. We show here that the expression of inflammatory cytokines is suppressed by IL-4 at the transcriptional level. Interleukin-4, when added together with bacterial lipopolysaccharide (LPS), suppressed LPS-induced increases in mRNA levels of IL-1α, IL-1β, IL-8, and TNF-α in alveolar macrophages. The level of suppression was dependent on dose and time of exposure and reached a maximum of 75–80% of uninduced values for IL-1α, IL-8, and TNF. Interleukin-1β expression was completely inhibited by IL-4. The amount of secreted protein, as determined by TNF-α bioassay, was also suppressed by IL-4. Half-maximal suppression occurred at IL-4 concentrations between 0.02 and 0.1 ng/ml for all inflammatory cytokines. Nuclear run-on assays showed that IL-4 suppressed transcriptional activity of all inflammatory cytokines. Messenger RNA stability was not changed by IL-4. The data suggest that IL-4 plays an important transcriptional role in the regulation of alveolar macrophage inflammatory activities in respiratory disease and raise the possibility that IL-4 may function in vivo as a coordinator of inflammatory and immune responses J. Leukoc. Biol. 56: 507–513; 1994.
Cytokine regulation of TNF-α mRNA and protein production by unprimed macrophages from C57BI/6 and NZW mice
Authors: Schook Lawrence B , Albrecht Hugo , Gallay Philippe , Jongeneel C Victor 
Published: January 2018

Abstract
It is well known that bacterial lipopolysaccharide (LPS) induces the synthesis of tumor necrosis factor α (TNF-α) and other inflammatory cytokines by primary monocytes and macrophages and that the Thl lymphokines, interleukin-2 (IL-2) and interferon-γ (IFN-γ), augment this response. We investigated the ability of IL-2 and IFN-γ to induce the production of TNF-α mRNA and protein independently of LPS and the modulation of this response by macrophage colony-stimulating factor (M-CSF) and IL-10. We found that IL-2 and IFN-γ were both able to induce the accumulation of TNF-α mRNA, albeit with slower kinetics than LPS, and that they acted synergistically. However, very little TNF bioactivity was secreted by lymphokine-stimulated macrophages unless LPS was also added. This finding underscores the importance of translational effects in the control of TNF production. M-CSF and IL-10 strongly inhibited TNF production at the level of both mRNA and bioactivity but had no effect on the production of IL-6. Bone marrow-derived or thiogycollate-elicited macrophages from the NZW mouse strain, which have been reported to be deficient in their ability to produce TNF, were at least as responsive to LPS or lymphokines as those taken from the C57B1/6 strain and were similarly affected by M-CSF and IL-10. Therefore, the genetic defect of NZW mice is not a primary deficiency in TNF production J. Leukoc. Biol. 56: 514–520; 1994.
IgE and eosinophil regulation in a murine model of allergic aspergillosis
Authors: Kurup Viswanath P , Choi Hongyung , Murali Pazhayannur S , Coffman Robert L 
Published: January 2018

Abstract
Exposure of BALB/c mice to Aspergillus fumigatus (Af), the antigen responsible for causing allergic bronchopulmonary aspergillosis in humans, caused elevated levels of serum immunoglobulin E (IgE) and peripheral blood and lung eosinophilia similar to that observed in the human disease. We have investigated the role of interleukin-4 (IL-4), IL-5 and interferon-γ in regulating IgE and eosinophilia in the mouse model. Animals were immunized by intraperitoneal injections of soluble Af antigens adsorbed to alum. These animals developed elevated IgE and Af specific IgG1 and were then treated with anticytokine monoclonal antibodies before the final exposure to particulate Af antigens by the intranasal route. The results showed that anti-IL-5 abrogated eosinophilia in mice, while those treated with anti-IL-4 retained the same or reduced IgE levels compared to pretreatment levels. All anti–IL-5, anti–IFN-γ, and control antibody–treated animals showed enhanced IgE levels. Anti–IFN-γ treatment of mice resulted in marked enhancement of eosinophilia compared to all other groups. Eosinophil numbers observed in the histological sections of the lungs confirmed the eosinophilia detected in the peripheral blood. These results indicate that the increase in IgE and eosinophils after exposure to Af antigens in BALB/c mice are due to Af-induced production of IL-4 and IL-5 and that both IgE and eosinophilia are independently regulated. J. Leukoc. Biol. 56: 593–598; 1994.
Dietary polyunsaturated fatty acid effects on immune cells of the porcine lung
Authors: Turek J J , Schoenlein I A , Clark L K , Van Alstine W G 
Published: January 2018

Abstract
The effects of various dietary polyunsaturated fatty acids (PUFAs) on the function of immune cells of the porcine lung was studied. Groups of six pigs were fed diets containing 10.5% corn oil [CO; enriched in linoleic acid (18:2, n-6)], linseed oil (LO; enriched in α-linolenic acid (18:3, n-3)], menhaden oil (MO; enriched in eicosapentaenoic (20:5; n-3) and docosahexaenoic (22:6; n-3) acids], linseed + corn oil (1:1; LC), and menhaden + corn oil (1:1; MC) for 28–30 days. Basal levels of alveolar macrophage (mφ) tumor necrosis factor-α (TNF-α) production were higher (P &lt; .05) for LC- and MC-fed pigs than for CO- and LO-fed pigs. Lipopolysaccharide (LPS)-stimulated LC and MC mφs produced more TNF than mφs from pigs fed CO, LO, and MO diets. Macrophages from pigs receiving the CO and LC diets had higher (P &lt; .05) levels of leucine aminopeptidase than mfs from the other dietary groups. Lipopolysaccharide did not increase mφ nitrite production over basal levels except in the MO diet group. However, LPS-stimulated mφs from the CO, MO, and LC dietary groups produced more nitrite than mfs from MC-fed pigs. Alveolar lymphocytes from pigs receiving the MC diet produced more T cell growth factors than LO and MO mφs. Alveolar mφs from the different dietary groups did not differ in their capacity for non-immune-mediated phagocytosis of fluorescent latex beads. These results indicate that dietary PUFAs can modulate some functions of porcine alveolar immune cells and that this may prove significant for host response to respiratory disease agents. J. Leukoc. Biol. 56: 599–604; 1994.
Hyaluronan receptor (CD44) expression and function in human peripheral blood monocytes and alveolar macrophages
Authors: Culty Martine , O’Mara Thomas E , Underhill Charles B , Yeager Henry , Swartz Rodney P 
Published: January 2018

Abstract
CD44 glycoproteins are present on the surfaces of many hematopoietic cells and in some cases can bind hyaluronan, a major component of the extracellular matrix. In the present study, we have found that newly explanted human peripheral blood monocytes (PBMs) exhibit a major CD44 band of 85 kDa, whereas autologous alveolar macrophages (AMφ) express multiple isoforms ranging from 85 to 200 kDa. Within 4 h in culture, PBMs began expressing new CD44 isoforms of 120, 150, and 180 kDa. Newly explanted AMφ specifically bound [3H]hyaluronan (135 cpm/μg protein), but newly explanted PBMs did not. However, in vitro cultured PBM progressively acquired the ability to bind [3H]hyaluronan and exhibited specific binding of hyaluronan similar to that of AMφ (113 cpm/μg protein) after 4 days in culture. In both cases, the binding of [3H]hyaluronan was specifically inhibited by the addition of monoclonal antibody directed against CD44. AMφ readily degraded [3H]hyaluronan and reached a plateau after 4 days in culture (115 cpm/μg protein). Newly explanted PBM exhibit no hyaluronan degradation and only a small degradative activity after 4 days in culture (6 to 11 cpm/μg protein). Thus, CD44 expression and function appear to change as PBM mature in vitro resembling more that found in AMφ. J. Leukoc. Biol. 56: 605–611; 1994.
Role for oxygen radicals in self-sustained HIV-1 replication in monocyte-derived macrophages: enhanced HIV-1 replication by N-acetyl-L-cysteine
Authors: Nottet Hans S L M , van Asbeck B Sweder , de Graaf Loek , de Vos N Machiel , Visser Maarten R , Verhoef Jan 
Published: January 2018

Abstract
N-acetyl-l-cysteine (NAC) has been proposed as a therapeutic agent for AIDS patients because it reduces human immunodeficiency virus type 1 (HIV-1) replication in stimulated T cells. However, NAC and glutathione enhanced acute HIV-1 replication in monocyte-derived macrophages. Buthionine sulfoximine did not affect NAC-mediated enhanced HIV-1 replication, indicating that the NAC-mediated effects are glutathione-independent. Superoxide dismutase and the hydroxyl radical scavengers dimethylthiourea and thiourea, but not urea, inhibited acute HIV-1 replication in macrophages. NAC reduced ferricytochrome c and increased dose-dependently Fe(III)-citrate and Fe(III)-EDTA-catalyzed hydroxyl radical formation in a system using glucose and glucose oxidase. Dimethylthiourea and thiourea, but not urea and superoxide dismutase, dose-dependently inhibited NAC-mediated enhancement of HIV-1 replication. These data suggest that oxygen radicals play an important role in self-sustained HIV-1 replication in macrophages and that oxygen radical scavengers other than NAC should be considered as therapeutic agents for AIDS patients. J. Leukoc. Biol. 56: 702–707; 1994.
Characterization of nitric oxide–stimulated ADP-ribosylation of various proteins from the mouse macrophage cell line ANA-1 using sodium nitroprusside and the novel nitric oxide-donating compound diethylamine dinitric oxide
Authors: Sheffler Lynn A , Wink David A , Melillo Giovanni , Cox George W 
Published: January 2018

Abstract
We examined the ability of nitric oxide (NO) to stimulate the ADP-ribosylation of proteins from the mouse macrophage cell line ANA-1. To demonstrate a specific effect of NO, we used a novel compound named diethylamine dinitric oxide (DEA/NO; l,l-diethyl-2-hydroxy-2-nitrosohydrazine, sodium salt; [Et2NN(O)NO]Na), which releases NO in aqueous solution at neutral pH. DEA/NO stimulated the ADP-ribosylation of at least three cytosolic proteins (Mr = 28,000, 33,000, and 39,000) from ANA-1 macrophages. The effect of DEA/NO on the ADP-ribosylation of the predominant target p39 was dose dependent (EC50 = 80 μM). Moreover, the effect of DEA/NO was attributed specifically to released NO rather than diethylamine or nitrite. Sodium nitroprusside (SNP) also stimulated the ADP-ribosylation of cytosolic proteins from ANA-1 mouse macrophages. However, SNP exhibited different time- and dose-dependent effects on the modification of p39. NO synthesized via the activity of interferon-γ plus lipopolysaccharide-induced NO synthase also enhanced the ADP-ribosylation of p39, confirming that the effects of DEA/NO and SNP could be attributed to NO or reactive nitrogen oxide species. Neither pertussis toxin nor cholera toxin stimulated the ADP-ribosylation of p39; however, cholera toxin stimulated the ADP-ribosylation of proteins with approximate molecular weights of 28,000 and 33,000. These data suggest that the induced expression of NO synthase in tumoricidal macrophages may be associated with autocrine and paracrine effects of NO that include the ADP-ribosylation of various proteins. Moreover, these results indicate that DEA/NO and related compounds may be useful as pharmacologic tools for investigating the effects of NO and reactive nitrogen oxide species on macrophages. J. Leukoc. Biol. 57: 152–159; 1995.
Differential effects of the anti-inflammatory compounds heparin, mannose-6-phosphate, and castanospermine on degradation of the vascular basement membrane by leukocytes, endothelial cells, and platelets
Authors: Bartlett Mark R , Cowden William B , Parish Christopher R 
Published: January 2018

Abstract
Recent studies suggest that heparin, mannose-6-phosphate (M6P), and castanospermine (CS) may mediate their anti-inflammatory effects by inhibiting the passage of leukocytes through the subendothelial basement membrane (BM). In order to test this hypothesis, heparin, M6P, and CS were examined for their ability to prevent the in vitro degradation of a 35SO4-labeled extracellular matrix (ECM) by neutrophils, lymphocytes, endothelial cells (ECs), and platelets, the labeled ECM degradation products being analyzed by gel filtration chromatography. All three compounds inhibited 35SO4-labeled ECM degradation, but M6P and CS were cell-type specific in their effects. Heparin inhibited the heparanase activity of all cell types examined, confirming the results of previous studies using similar in vitro techniques. M6P selectively inhibited lymphocyte heparanase but not that of platelets, neutrophils, or ECs. CS selectively inhibited phorbol myristate acetate (PMA)-induced EC heparanase and sulfatase activity but did not affect the constitutive expression of degradative enzymes by non-stimulated ECs. These findings provide important clues to the mode of action of these compounds and the characteristic inflammatory pathology associated with the use of each anti-inflammatory agent. In particular, the data support the view that leukocytes markedly differ in the mechanisms they use to degrade BM/ECM to enable extravasation and that some degree of cooperation with EC is required in this process. J. Leukoc. Biol. 57: 207–213; 1995.
Functional deficiencies in two distinct interferon α-producing cell populations in peripheral blood mononuclear cells from human immunodeficiency virus seropositive patients
Authors: Feldman Stephen B , Milone Michael C , Kloser Patricia , Fitzgerald-Bocarsly Patricia 
Published: January 2018

Abstract
Two populations of IFN-α producing cells (IPC) were examined to determine whether they are coordinately dysregulated in human immunodeficiency virus (HIV) disease. IFN-α produced in response to herpes simplex virus (HSV) and Sendai virus (SV) was measured and the frequencies of the IPC were obtained by ELISpot assay. IPC that respond to HSV (natural IFN-α producing cells) and those responding to SV (predominantly monocytes) were present, on average, at 7.6 and 138 per 104 PBMC in healthy controls, respectively. More patients had a reduced IFN-α response to HSV than to SV, and individual patients did not show a decreased response to SV without a decreased response to HSV. Neither IPC function was correlated with CD4+ cell levels. We conclude that the defects in IFN-α production in these two cell populations arise independently, possibly due to differences in susceptibility to HIV infection or molecular regulation. J. Leukoc. Biol. 57: 214–220; 1995.