bluuebunny/crossref_metadata_2025_split huggingface dataset:
Costimulatory molecules CD80 and CD86 in the rat; tissue distribution and expression by antigen-presenting cells
Authors: Damoiseaux Jan G M C , Yagita Hideo , Okumura Ko , van Breda Vriesman Peter J C 
Published: January 2018

Abstract
The CD28-CD80/CD86 costimulatory pathway provides a critical signal for T cell activation. Only recently rat CD80 and CD86 have been cloned and monoclonal antibodies have been generated. In this study we examined the expression of these molecules in lymphoid tissue and on purified subsets of antigen-presenting cells (APC). The target tissue of cyclosporin A-induced autoimmunity, i.e. the skin and tongue, were also examined for expression of CD80 and CD86. Whereas CD80 was hardly detected in the lymphoid tissues, CD86 was clearly expressed by non-lymphoid cells in the thymus, as well as in the secondary lymphoid organs. With respect to lymphoid cells, only germinal center B cells exhibited clear CD86 expression. Phenotypic analysis by flow cytometry revealed that only dendritic cells, both of thymic and splenic origin, expressed the full array of stimulatory molecules required for the proper activation of naive T cells. On development of cyclosporin A-induced autoimmunity, non-professional APC, i.e. epithelial cells, started to express MHC class II, but not the costimulatory ligands CD80 and CD86. However, CD86 staining was observed in the target tissue and was associated with Langerhans cells as well as infiltrating leukocytes. Altogether, our results show that also in the rat strong stimulatory capacity for primary immune responses is associated with the expression of the costimulatory ligands CD80 and CD86. As concluded from the in situ expression CD86 may be the predominant costimulatory ligand early in immune responses. J. Leukoc. Biol. 64: 803–809; 1998.
Lipopolysaccharide can block the potential of monocytes to differentiate into dendritic cells
Authors: Palucka Karolina A , Taquet Nicolas , Sanchez-Chapuis Francoise , Gluckman Jean Claude 
Published: January 2018

Abstract
We examined whether priming monocytes (MO) with lipopolysaccharide (LPS) influenced their further differentiation into either macrophages (MÕ) or dendritic cells (DC). LPS-primed MO differentiated into MÕ when cultured further with MÕ colony-stimulating factor (M-CSF) but, if cultured then with granulocyte/MÕ (GM)-CSF and IL-4 (interleukin-4), only about 30% of the cells differentiated into CD1a+CD14− DC and half became CD1a−CD14+ MÕ. Cytokines present during LPS priming could affect subsequent MO differentiation. Relative to priming with LPS alone, adding M-CSF to LPS did not modify differentiation of MO to MÕ in further culture with M-CSF, nor did it change the way of differentiation of MO into DC was altered if culture was later switched to GM-CSF/IL-4. Using GM-CSF/IL-4 plus LPS upon priming did not modify differentiation of MO to MÕ in further culture with M-CSF, as compared to priming with GM-CSF/IL-4 alone, but it counteracted the effect of LPS on the differentiation of MO to DC in further culture with GM-CSF/IL-4: about 75% of cells then became DC. Alternatively, despite activation by LPS, mature M-CSF-induced MÕ preserved the potential to differentiate into DC on subsequent culture with GM-CSF/IL-4. Thus, LPS, a bacterial product known to sustain maturation of MO/MÕ as well as of DC, may block the differentiation of MO into DC, except if signal triggering DC differentiation is delivered concomitantly, and modulate in this manner the induction of adaptive immune responses to infection. J. Leukoc. Biol. 65: 232–240; 1999.
TALL-1 is a novel member of the TNF family that is down-regulated by mitogens
Authors: Shu Hong-Bing , Hu Wen-Hui , Johnson Holly 
Published: January 2018

Abstract
Members of the tumor necrosis factor (TNF) family play important roles in modulation of immune responses. We describe the identification and cloning of a novel TNF family member that has been designated as TALL-1. TALL-1 is a 285-amino acid type II transmembrane protein. Its carboxy terminus shares ∼35% sequence identity with the recently identified APRIL and ∼20–25% with TNF, FasL, TRAIL, and lymphotoxin-α, suggesting that TALL-1 and APRIL belong to a subfamily of the TNF family of ligands. Northern blot analysis suggests that TALL-1 is expressed abundantly in peripheral blood leukocytes and weakly in spleen but is barely detectable in all other tissues examined. Reverse transcriptase-polymerase chain reaction analysis indicates that TALL-1 is specifically expressed in monocytes and macrophages but is undetectable in T and B lymphocytes. Furthermore, TALL-1 expression is dramatically down-regulated by phorbol myristate acetate/ionomycin. J. Leukoc. Biol. 65: 680–683; 1999.
Substance P primes the formation of hydrogen peroxide and nitric oxide in human neutrophils
Authors: Sterner-Kock Anja , Braun Ruedi K , van der Vliet Albert , Schrenzel Mark D , McDonald Ruth J , Kabbur Mahendra B , Vulliet P Richard , Hyde Dallas M 
Published: January 2018

Abstract
Substance P (SP), a neurotransmitter of the central and peripheral nervous system, has been implicated as a mediator of the pulmonary inflammatory response through its stimulatory effects on neutrophils. We investigated the role of SP in priming the production of reactive oxygen species by human neutrophils with the cytochrome c reduction assay and by flow cytometry using the intracellular oxidizable probe dichlorofluorescein. We also investigated SP-induced formation of nitrite and nitrate as an index of nitric oxide (NO) production. Our results indicate that SP primes two distinct pathways with respect to the induction of reactive oxygen species in the human neutrophil: the production of superoxide anion and hydrogen peroxide by the calmodulin-dependent NADPH oxidase, and the generation of NO by a constitutive NO synthase. Preincubation of neutrophils with inhibitors of calmodulin and NO synthase diminished the oxidative response in an additive fashion. These results give insight into distinct signal transduction pathways in the SP-primed neutrophil with respect to the formation of superoxide anion, hydrogen peroxide, and NO. J. Leukoc. Biol. 65: 834–840; 1999.
ETS transcription factors regulate an enhancer activity in the third intron of TNF-α
Authors: Tomaras Georgia D , Foster Dalton A , Burrer Christine M , Taffet Steven M 
Published: January 2018

Abstract
We describe an enhancer site in the third intron of tumor necrosis factor α (TNF-α). A reporter construct containing the 5′-flanking region of the mouse TNF-α gene displayed weak activity when transfected into RAW264.7 macrophage-like cells. The addition of the third intron of TNF-α to this construct resulted in an enhancement of CAT protein. This enhancement was eliminated if a conserved 20-bp sequence was removed from the intron or if a dominant-negative ets-binding factor was co-transfected with the reporter gene. Mutations of this site that destroyed potential ets transcription factor binding sites had reduced transcriptional activity. The major transcription factor that bound to the oligonucleotide was confirmed to be GABP by supershift and competition analysis. In RAW264.7 cells, the binding was constitutive, however, in bone marrow-derived macrophages binding activity was shown to be interferon-γ inducible. This may imply a role for ets transcription factors in the production of TNF-α. J. Leukoc. Biol. 66: 183–193; 1999.
Reperfusion-induced oxidative stress in diabetes: cellular and enzymatic sources
Authors: Salas A , Panés J , Elizalde J I , Granger D N , Piqué J M 
Published: January 2018

Abstract
Reactive oxygen metabolites (ROMs) have been implicated in the pathogenesis of the inflammatory response to ischemia/reperfusion (I/R), which is exacerbated in diabetes. This study revealed an increased (P &lt; 0.01) ROMs production in mesenteric tissue (measured using the oxidant-sensitive fluorochrome dihydrorhodamine 123) after I/R in control and diabetic rats, with larger increments (P &lt; 0.0001) observed in the latter group, that was associated with an increased inflammatory response measured by intravital microscopy. Either xanthine oxidase inhibition, superoxide scavenging, ICAM-1 immunoneutralization, or blockade of platelet-activating factor or leukotrienes effectively reduced leukocyte recruitment and ROMs production in control and diabetic rats. Moreover, neutrophils from diabetic rats showed an enhanced production of ROMs in vitro in basal and stimulated conditions. We conclude that the oxidative stress during reperfusion is markedly enhanced in diabetes and this appears to result from increased leukocyte recruitment and a higher capacity of diabetic leukocytes to generate ROMs in response to stimulation. J. Leukoc. Biol. 66: 59–66; 1999.
Decreased availability of GDP-l-fucose in a patient with LAD II with normal GDP-d-mannose dehydratase and FX protein activities
Authors: Körner C , Linnebank M , Koch H G , Harms E , von Figura K , Marquardt T 
Published: January 2018

Abstract
Leukocyte adhesion deficiency type II (LAD II) is caused by a disorder in the metabolism of GDP-l-fucose, which causes hypofucosylation of glycoconjugates. This study analyzes a newly identified LAD II patient who shows the same severe hypofucosylation of glycoconjugates as the other described patients. However, in vitro assays of cytosolic extracts from leukocytes and fibroblasts of the patient demonstrated a normal GDP-l-fucose biosynthesis from GDP-d-mannose. Analysis of the two enzymes involved in the pathway, GDP-d-mannose 4,6-dehydratase and FX protein, revealed normal numbers of transcripts without any detectable mutations within the coding regions of either gene. In contrast to previously published observations [Sturla et al. (1998) FEBS Lett. 429, 274–278], the major pathway of GDP-l-fucose synthesis can be normal in LAD II. J. Leukoc. Biol. 66: 95–98; 1999.
Myeloid dendritic cells
Authors: Steinman Ralph M , Inaba Kayo 
Published: January 2018

Abstract
There is considerable but as yet incomplete evidence for two developmental lineages of dendritic cells: a myeloid lineage shared with phagocytes and a lymphoid lineage shared with T cells. The two corresponding functional states, which may not require the existence of two formal lineages, are that myeloid dendritic cells capture antigens in the periphery and then migrate to the lymphoid organs to initiate immunity, whereas lymphoid dendritic cells are found in the thymic medulla and lymph node T cell areas and are responsible for tolerance. The latter may occur through immune regulation and/or deletion. Myeloid dendritic cells undergo many activities that contribute to the initiation of immunity. These are summarized here and include mobilization from progenitors and precursors in the blood and marrow, maturation from immature cells in the skin and interstitial spaces, formation of MHC-peptide complexes in MHC class II compartments or MIICs, migration to the T cell areas, and finally, mortality. The death of migratory dendritic cells seems to be accompanied by their phagocytosis and processing by other dendritic cells in the T area. We speculate that this transfer of antigens, including self-peptides captured by the uptake of apoptotic cells in peripheral tissues, is an important prelude to the regulatory function of resident or lymphoid dendritic cells in the T cell area. These features of dendritic cell biology provide targets to manipulate the immune response in vivo. J. Leukoc. Biol. 66: 205–208; 1999.
Donor dendritic cell persistence in organ allograft recipients in the absence of immunosuppression
Authors: O'Connell Peta J , Burlingham William J 
Published: January 2018

Abstract
Donor-derived leukocytes are known to persist in the peripheral blood of organ allograft recipients after withdrawal of all immunosuppressive drug therapy and can exert a donor-specific veto effect. Antigen-presenting cells (APC), in particular dendritic cells (DC), have been proposed as a candidate for this veto leukocyte. Myeloid DC were derived from the peripheral blood of two non-compliant organ transplant recipients: D. S., a heart transplant recipient, and J. M., a liver transplant recipient. Donor-specific signal was enriched in the cultured DC fraction relative to whole blood for both patients. The clinical outcome in each patient was different: D. S. lost his heart allograft due to biopsy-proven acute and chronic rejection 2.5 years after discontinuing anti-rejection medication; J. M. continues to maintain adequate liver function. The results have important implications for the planned withdrawal of immunosuppression in tolerance protocols as DC may play a role either in the maintenance of tolerance or immune activation. J. Leukoc. Biol. 66: 301–305; 1999.
Annexins VII and XI are present in a human macrophage-like cell line. Differential translocation on FcR-mediated phagocytosis
Authors: Pittis M G , Garcia R C 
Published: January 2018

Abstract
We have studied the divalent cation-dependent association of proteins to subcellular fractions of human macrophage-like cells before and after FcR-mediated phagocytosis. Among these proteins we have identified annexins VII and XI for the first time in these cells, along with annexins I, III, and VI. Although all of these annexins are present in the cytosolic fraction, the extent of their association to membrane and phagosome fractions from resting and stimulated cells is variable. Annexin VII translocates from cytosolic to membrane fractions after phagocytic stimulation, along with annexin I, III, and VI. Annexins VII and XI are found associated with purified phagosomes along with I, III, and VI, and this association is greater after a 24-h chase period. Our results show differences in the intracellular distribution of different annexins in macrophage-like cells on phagocytosis. Annexins VII, VI, III, and I respond to particle ingestion by translocating to phagosomes and other cell membrane structures, whereas annexin XI translocates predominantly to phagosomes, suggesting dissimilarities in their function. J. Leukoc. Biol. 66: 845–850; 1999.
Role of IFN-γ on dissociation between nitric oxide and TNF/IL-6 production by murine peritoneal cells after restimulation with bacterial lipopolysaccharide
Authors: Tominaga Kaoru , Saito Shinji , Matsuura Motohiro , Funatogawa Keiji , Matsumura Haruo , Nakano Masayasu 
Published: January 2018

Abstract
Murine peritoneal exudate cells (PEC) pre-exposed to bacterial lipopolysaccharide (LPS) show augmented nitric oxide (NO) production by LPS restimulation, in contrast to LPS tolerance with reduced production of tumor necrosis factor α (TNF-α) and interleukin-6 (IL-6). Significant amounts of interferon-γ (IFN-γ) were detected in the PEC cultures on LPS stimulation, and anti-IFN-γ antibody suppressed the LPS-induced NO, but not TNF-α and IL-6, production. Addition of anti-IFN-γ antibody to the cultures in the LPS pre-exposure step strongly suppressed the augmented NO production on LPS restimulation. Anti-IL-12 antibody, which suppressed the LPS-induced IFN-γ production, also suppressed the augmented NO production, as did anti-IFN-γ antibody. Taken together, we propose the following mechanisms: (1) T and NK cells in PEC produce IFN-γ by the action of IL-12, which is derived from LPS-stimulated macrophages, and (2) the de novo-produced IFN-γ activates macrophages to augment NO production on LPS restimulation. J. Leukoc. Biol. 66: 974–980; 1999.
Platelet-activating factor activates mitogen-activated protein kinases through the activation of phosphatidylinositol 3-kinase and tyrosine kinase in human eosinophils
Authors: Miike Satoshi , Kurasawa Kazuhiro , Saito Yasushi , Iwamoto Itsuo 
Published: January 2018

Abstract
We determined whether platelet-activating factor (PAF) activates mitogen-activated protein (MAP) kinases in human eosinophils, and if so, which signaling pathways are utilized for the MAP kinase activation. PAF activated 42-and 44-kDa MAP kinases (ERK1/ERK2) in eosinophils, which became maximal at 1 min after stimulation. The PAF receptor antagonist E6123 and pertussis toxin inhibited the PAF-induced MAP kinase activation in eosinophils. The phosphatidylinositol 3-kinase (PI 3-kinase) inhibitor wortmannin, tyrosine kinase inhibitors herbimycin A and genistein, and an intracellular Ca2+ chelator BAPTA/AM inhibited PAF-induced MAP kinase activation in eosinophils, whereas protein kinase C inhibitors staurosporine and calphostin C had no effect. Furthermore, wortmannin as well as herbimycin A and genistein, but not BAPTA/AM, prevented PAF-induced tyrosine phosphorylation of Shc adapter protein in eosinophils. Finally, the specific MEK inhibitor PD98059 inhibited PAF-induced chemotaxis in eosinophils. Taken together, these results indicate that PAF activates MAP kinases in eosinophils through the activation of PI 3-kinase and a tyrosine kinase and the increase in intracellular Ca2+ and that PAF-induced MAP kinase activation mediates chemotaxis in eosinophils. J. Leukoc. Biol. 67: 117–126; 2000.
A novel lysophosphatidic acid analog, LXR-1035, inhibits leukocyte-endothelium interaction via inhibition of cell adhesion molecules
Authors: Scalia Rosario , Pruefer Diethard , Lefer Allan M 
Published: January 2018

Abstract
A novel synthetic phosphorothioate analog of oleoyl lysophosphatidic acid LXR-1035 was studied for its ability to modulate leukocyte-endothelial cell interactions using intravital microscopy of the rat mesentery. Superfusion of the rat mesentery with 50 μM l-NAME elicited a significant, time-dependent increase in leukocyte rolling, adherence, and transmigration compared to control rats superfused with Krebs-Henseleit solution. However, superfusion of the rat mesentery with 300 nM LXR-1035 consistently attenuated 65–87% of the l-NAME-induced leukocyte rolling, adherence, and transmigration, without altering systemic blood pressure or mesenteric venular shear rate. Similar results were also obtained in rats subjected to 90 min of hemorrhage followed by 90 min of reperfusion. Resuscitation from hemorrhage increased significantly the number of rolling, adherent, and transmigrated leukocytes in the rat mesenteric microcirculation. However, superfusion of the rat mesentery with LXR-1035 markedly attenuated the leukocyte-endothelium interaction occurring after hemorrhage and reinfusion by 75 ± 12%. Immunohistochemical localization of P-selectin expression on mesenteric venular endothelium was significantly increased after exposure to l-NAME and after hemorrhage-reinfusion, which was significantly attenuated by LXR-1035 (P &lt; 0.05). In addition, treatment of isolated rat neutrophils with 300 nM LXR-1035 significantly attenuated leukotriene B4-induced up-regulation of CD18 (P &lt; 0.05). Our data clearly demonstrate that LXR-1035 can potently inhibit the recruitment of leukocytes in the mesenteric rat microvasculature by attenuating cell-surface expression of adhesion molecules. J. Leukoc. Biol. 67: 26–33; 2000.
Human monocytic U937 cells transfected with human hepatic inducible nitric oxide synthase exhibit leishmanicidal activity
Authors: Bertholet Sylvie , Mauël Jacques 
Published: January 2018

Abstract
In mice, the high inducible synthesis of nitric oxide (NO) resulting from inducible NO synthase (iNOS, NOS2) expression by macrophages (M) is considered an essential component of the protective immune response against infection by intracellular pathogens. Conversely, in humans, the question of a role for NO as an antimicrobial defense mechanism has been the subject of much debate. Recently, however, iNOS expression by human M and formation of NO or its derivatives have been reported both in vivo and in vitro, strongly suggesting that human M are indeed capable of inducible NO synthesis. However, the conditions allowing NO production by human M in culture remain poorly defined, rendering more difficult the study of the effector functions of NO in these cells. To alleviate this problem, cells of the U937 monocytoid line were engineered to express iNOS by transfection with human hepatic iNOS (DFGiNOS), leading to production of NO on supplementation with the cofactor tetrahydrobiopterin. We report that U937 cells, when differentiated with 1,25-dihydroxyvitamin D3 and retinoic acid, acquire a phenotype allowing infection by Leishmania parasites and maintain viable intracellular microorganisms up to 72 h post-infection. Leishmania survival in DFGiNOS cells is strongly decreased when the cells are treated with tetrahydrobiopterin. Intracellular killing is evident by 24 h and increases up to 72 h post-infection, and is inhibited by L-N 5-(1-iminoethyl)ornithine, an inhibitor of NO synthesis. In contrast, superoxide anion does not appear to play a role in the killing of Leishmania by DGFiNOS U937 cells. The relevance of this model to the study of the mechanisms of intracellular killing by human macrophages is discussed. J. Leukoc. Biol. 67: 34–39; 2000.
TNF-α release by monocytic THP-1 cells through cross-linking of the extended V-region of the oral streptococcal protein I/II
Authors: Chatenay-Rivauday Christian , Yamodo Innocent , Sciotti Michel-Angelo , Troffer-Charlier Nathalie , Klein Jean-Paul , Ogier Joelle A 
Published: January 2018

Abstract
We tested the hypothesis of a conserved activation mode of monocytic THP-1 cells by proteins I/II expressed by several species of oral streptococci through the specific role of the extended V-region. We studied the binding and modulating activities of six proteins I/II purified from strains representing four different species of oral streptococci, and of expression products of polymerase chain reaction-amplified sequences encoding corresponding extended V-regions. We found that the different proteins I/II bound to THP-1 cells in a sugar-dependent mode involving the extended V-region. Furthermore, all the proteins I/II stimulated THP-1 cells to produce tumor necrosis factor α, indicating that these properties are not strain- or species-specific. Despite the weak stimulation of THP-1 cells by the extended V-region alone, we obtained evidence that cross-linking of this region can be one of the mechanisms involved in monocytic cell activation by proteins I/II. J. Leukoc. Biol. 67: 81–89; 2000.
Serglycin secreted by leukocytes is efficiently eliminated from the circulation by sinusoidal scavenger endothelial cells in the liver
Authors: øynebråten Inger , Hansen Berit , Smedsrød Bård , Uhlin-Hansen Lars 
Published: January 2018

Abstract
This study was undertaken to determine the fate of the circulating chondroitin sulfate proteoglycan serglycin. The human monocytic cell line THP-1 was cultured under serum-free conditions in the presence of [35S]sulfate. The conditioned medium was harvested and S-macromolecules were purified by Q-Sepharose anion-exchange chromatography and Superose 6 gel chromatography. After labeling with 12I, the purified material was treated with chondroitinase ABC and subjected to sodium dodecyl sulfate polyacrylamide gel electrophoresis. A major band with mr of approximately 14 kDa appeared, consistent with the core protein of serglycin. The identity of the proteoglycan was confirmed by amino-terminal amino acid sequencing. Purified serglycin, labeled either with [35S]sulfate or 125I and fluorescein isothiocyanate, was injected intravenously into rats. The blood content of radiolabeled serglycin fell by 50% from 1 to 2.4 min after injection, indicating an initial t1/2 of 1.4 min or shorter. Approximately 90% of the recovered radioactivity was localized in the liver, 5% in the blood, and 5% altogether in urine, kidneys, and spleen about 30 min after injection. Isolation of liver cells at the same time point showed that 70% of the radioactivity was taken up by the sinusoidal scavenger endothelial cells, and 23 and 7% by the hepatocytes and Kupffer cells, respectively. When excess amounts of unlabeled hyaluronan was co-injected with radiolabeled serglycin, the elimination of serglycin was significantly inhibited, indicating that the hyaluronan receptor on the sinusoidal scavenger endothelial cells is responsible for the elimination of serglycin. J. Leukoc. Biol. 67: 183–188; 2000.