bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characterization of the eosinophil granule proteins recognized by the activation-specific antibody EG2
Authors: Rosenberg Helene F , Lee Tiffany H 
Published: January 2018

Abstract
Monoclonal antibodies EG1 and EG2 have the unique ability to distinguish the storage from the secreted forms of the eosinophil cationic protein (ECP). EG2 has been used extensively as a marker for activated, secreting eosinophils, despite the fact that no biochemical differences between the storage and secreted forms of ECP have been identified. We have determined that the activation-specific EG2 detects only one of three distinct glycosylated forms of ECP (18 kDa); in contrast, both EG1 and polyclonal anti-ECP antiserum can detect three glycosylated forms of this protein (18, 20, and 22 kDa). We have also determined that EG2 detects fully deglycosylated ECP as well as fully deglycosylated eosinophil-derived neurotoxin. Our results indicate that activation-specific EG2 recognizes a polypeptide epitope that is masked in the higher-molecular-weight, more heavily glycosylated forms of ECP. These findings suggest that deglycosylation may occur in conjunction with activation and secretion; alternatively, the 18-kDa form of ECP may be present in the storage granule of resting eosinophils but may remain undetected in an inaccessible location or conformation. J. Leukoc. Biol. 56: 502–506; 1994.
Cellular depletion of p56lck during thymocyte apoptosis
Authors: Garcia-Welsh Adrienne , Laskin Debra L , Shuler Randy L , Laskin Jeffrey D 
Published: January 2018

Abstract
The src-related protein tyrosine kinase p56lck is thought to be important in regulating maturation and functional responsiveness of T cells and thymocytes. In the present studies we report that expression of p56lck is suppressed during apoptosis. Using primary cultures of rat thymocytes, we found that agents that are effective in inducing apoptosis, including okadaic acid, dexamethasone, and antibodies to the CD3 receptor, also deplete cells of p56lck. This process is rapid, occurring within 24 h, and is not due to cytotoxicity. Inhibition of DNA fragmentation in apoptotic cells with the endonuclease inhibitor ZnCl2 failed to prevent depletion of p56lck, suggesting that it was not a consequence of the DNA degradation process. Using the thymic lymphoma cell line LSTRA, apoptosis was also associated with cellular depletion of p56. In contrast to thymocytes, this process required 48–72 h possibly because these cells overexpress p56lck. Although at this time we are uncertain as to the precise role of p56lck in the process of apoptosis, our results indicate that changes in the expression of this protein in thymocytes is an important marker of programmed cell death. J. Leukoc. Biol. 56: 528–532; 1994.
Establishment of the role of IL-6 and TNF receptor 1 using gene knockout mice
Authors: Bluethmann Horst , Rothe Joachim , Schultze Nathalie , Tkachuk Maria , Koebel Pascale 
Published: January 2018

Abstract
Cytokines are known to be key players in host response to infection, immunological disorders, and tissue injury in the attempt of an organism to overcome the insult and restore homeostasis. Another important aspect of cytokines, however, is their normal physiological role during development in the unchallenged organism. The most elegant way to analyze both of these functions is to introduce targeted mutations in embryonic stem cells in order to create new mouse strains deficient for a given cytokine and identify the functions that are consequently impaired or lost, This review summarizes the mutant phenotypes of mice carrying a null mutation in the cytokine IL-6 gene or the tumor necrosis factor receptor 1 (Tnfr1) gene. Results for interferon– and interferon-γ receptor-deficient mice are included for comparison. J. Leukoc. Biol. 56: 565–570; 1994.
Effects of fatty acids on proliferation and activation of human synovial compartment lymphocytes
Authors: DeMarco Deborah M , Santoli Daniela , Zurier Robert B 
Published: January 2018

Abstract
The object of this study was to determine the effects of eicosanoid precursor fatty acids on activation and proliferation of T lymphocytes from synovial fluid and synovial tissue of rheumatoid arthritis patients. Proliferation was determined by direct cell counts; phenotypic characterization of surface molecules was by cytofluorometric analysis. Dihomogammalinolenic acid, arachidonic acid, and eicosapentaenoic acid suppressed proliferation of interleukin-2-dependent lymphocytes by as much as 80%; cell viability was not altered by fatty acids. Administration of particular fatty acids may prove to be a useful therapeutic intervention in rheumatoid arthritis patients because of their ability to suppress activation and proliferation of synovial compartment T lymphocytes. J. Leukoc. Biol. 56: 612–615; 1994.
Delivery of exogenous antigen into the major histocompatibility complex class I and class II pathways by electroporation
Authors: Li Ying , Ke Yong , Gottlieb Paul D , Kapp Judith A 
Published: January 2018

Abstract
Exogenous, nonreplicating protein antigens (Ags) are usually taken up by antigen-presenting cells (APCs) via endocytosis or pinocytosis and enter the major histocompatibility complex (MHC) class II processing and presentation pathway. Although exogenous Ags are not processed and presented in the class I pathway by most cells, soluble proteins can enter the class I processing and presentation pathway if they are introduced directly into the cytoplasm of APCs. The purpose of these studies was to determine whether exogenous proteins could be processed and presented to T cells if they were delivered into cells by electroporation. The conditions for electroporation were optimized so that the viability of the electroporated cells was high, and the majority of electroporated cells had protein incorporated. Electroporated B cells not only presented exogenous ovalbumin to CD8+, class I MHC–restricted T cells but also stimulated CD4+, class II MHC–restricted T cells. Electroporated cells also primed Ag-specific cytotoxic T lymphocytes (CTLs) in vivo, stimulated CTL precursors in vitro, and served as target cells for lysis by Ag-specific CTLs, indistinguishable from transfected cells. Thus, electropermeabilized cells were structurally intact, and the introduced exogenous protein was processed and presented in association with both class I and class II MHC molecules. This approach is as efficient and reproducible as other techniques of delivering exogenous proteins into the intracellular processing pathways. These studies suggest that electroporation could be employed for the study of cell-mediated immunity to various exogenous proteins. J. Leukoc. Biol. 56: 616–624; 1994.
Cellular composition of Corynebacterium pseudotuberculosis pyogranulomas in sheep
Authors: Pépin Michel , Pittet Jean-Christophe , Olivier Michel , Gohin Isabelle 
Published: January 2018

Abstract
The cellular composition of 46 pyogranulomas experimentally induced with Corynebacterium pseudotuberculosis in sheep was determined by immunohistochemistry. Lesions localized in inoculation sites or draining lymph nodes consisted of macrophage and lymphocyte layers distributed around a necrotic center and surrounded by a fibrous capsule. In immature lesions, T cells of the CD4+ subset predominated, whereas in mature lesions proportions of CD8+ T lymphocytes and cells expressing the γ/δ chains for the T cell receptor increased. Numerous pyogranuloma cells expressed the interleukin-2 receptor. In addition to these general characteristics, a large individual variability in the proportions of macrophage and T cell subsets was observed for lesions of the same age, in particular for epithelioid macrophages. This heterogeneity suggests a different cellular pattern in relation to the persistence or the elimination of bacteria by the host. J. Leukoc. Biol. 56: 666–670; 1994.
Lipopolysaccharide and splenic tumoricidal macrophage activation
Authors: Verstovsek Srdan , Zaleskis Gintaras , Maccubbin Darbie L , Mihich Enrico , Ehrke M Jane 
Published: January 2018

Abstract
Splenic macrophage tumoricidal activity was examined and a splenic macrophage tumoricidal assay was established. Initially, mixtures of lipopolysaccharide (LPS) and spleen single cell suspensions (SSCS) were cultured for 1–4 days. Adherent macrophages, washed free of nonadherent cells and LPS, were then examined and were found to lack tumoricidal activity in a standard 18-h 51Cr release assay. However, tumoricidal activity was generated if LPS was added to the SSCS cultures at later time points during the 4-day incubation period; maximal activity was seen when LPS was added on day 3. In parallel, significant changes in macrophage autofluorescence and morphology, but not phenotype, were observed. Next, SSCS were cultured for 1–4 days without stimulating agents. Adherent macrophages were then washed free of nonadherent cells and LPS was added. Significant tumoricidal activity developed in time- and LPS concentration-dependent fashions. The presence of nonadherent spleen cells in physical contact with the macrophages during the SSCS culture was essential for the macrophages in the resultant monolayer to be responsive to LPS. Activated splenic macrophage-mediated lysis of tumor cells was shown to depend on the contact between the two cells. J. Leukoc. Biol. 56: 714–722; 1994.
Cellular target of in vitro–induced suppressor cells derived from the spleen of Mycobacterium lepraemurium–infected mice and role of IFN-γ in their development
Authors: Gosselin Diane , Turcotte Raymond , Lemieux Suzanne 
Published: January 2018

Abstract
Unfractionated spleen cells from C3H mice infected a few weeks before with Mycobacterium lepraemurium developed a suppressor activity after overnight culture. This requires contact of plastic adherent cells with nonadherent cells distinct from T, B, or natural killer cells. The present study demonstrates that anti-interferon-γ (IFN-γ) monoclonal antibody and indomethacin totally abrogate the expression, although not the induction, of this activity. Furthermore, culture-induced suppressor cells selectively inhibit T lymphocyte proliferation, probably by altering the generation of interleukin-2 (IL-2) responsiveness through reduction of the affinity and density of high-affinity IL-2 receptors on activated cells. These and other previously determined properties of culture-induced suppressor cells, similar to those of adherent suppressor cells detected in freshly harvested spleen cells at a later stage of M. lepraemurium infection, suggest a common precursor. If so, the present observations should help in defining a strategy to prevent the impairment of cell-mediated immunity in infected mice. J. Leukoc. Biol. 57: 122–128; 1995.
Polar agents with differentiation inducing capacity potentiate tumor necrosis factor-mediated cytotoxicity in human myeloid cell lines
Authors: Depraetere Stany , Vanhaesebroeck Bart , Fiers Walter , Willems Jean , Joniau Marcel 
Published: January 2018

Abstract
Cotreatment or pretreatment of several human myeloid cell lines (KG1, HL60, U937, THP1) with the differentiation inducer DMSO was found to potentiate the antiproliferative and cytotoxic effects of TNF. In addition, TNF-resistant monocytic cell lines could be sensitized to TNF cytotoxicity by DMSO treatment. Other highly polar molecules, known to be potent differentiation inducers, showed similar effects to those of DMSO. The potentiating effect of DMSO was related neither to an up-regulation of TNF receptor expression nor to an alteration in the rate of TNF internalization and degradation. We present evidence that the TNF activities are p55 TNF receptor-mediated and are not due to insertion of TNF into lipid bilayers, an effect that could be susceptible to DMSO, as this component has been described to modify cell membrane characteristics. DMSO-induced potentiation of TNF cytostasis/cytotoxicity was restricted to myeloid leukemia cell lines. In non-myeloid cells such as fibrosarcomas, myosarcomas, thymomas, or carcinomas, DMSO was found either not to alter or to inhibit TNF-induced cell death. The latter results are in good agreement with data reported by others who suggested that DMSO could act as a scavenger of TNF-induced toxic radical formation. The potential correlation in myeloid cells between DMSO-induced changes in the cells’ differentiation status and DMSO-enhanced TNF-susceptibility is discussed. J. Leukoc. Biol. 57: 141–151; 1995.
Expression of glycophosphatidylinositol-anchored and-non-anchored isoforms of vascular cell adhesion molecule 1 in murine stromal and endothelial cells
Authors: Kinashi Tatsuo , Pierre Yves St , Springer Timothy A 
Published: January 2018

Abstract
Monoclonal antibodies to murine vascular cell adhesion molecule-1 (VCAM-1, CD106) revealed not only the expected VCAM-1 molecule with an apparent molecular weight of 100 kDa, but also a molecule with a smaller size of 46 kDa in stromal cells and stimulated endothelial cells. Peptide mapping suggested the 46 kDa and 100 kDa proteins were closely related. The 46 kDa, but not 100 kDa protein, was cleaved from the cell surface with phosphatidylinositol-specific phospholipase C (PI-PLC), showing that the 46 kDa protein was a GPI-linked molecule. The 46 kDa and 100 kDa isoforms of VCAM-1 were shown to be N-glycosylated, have similar kinetics of biosynthesis, and to be partially shed from the cell surface with a slight reduction of size. TNF-α induced both isoforms of VCAM-1 with a similar time course of appearance on the surface of endothelial cells. The relative amounts of the 46 kDa and 100 kDa isoforms depended on the cell type examined. The GPI-anchored isoform is functionally important, because on a cell on which it was expressed almost as well as the 100 kDa isoform, treatment with PI-PLC reduced VLA-4-dependent conjugate formation. J. Leukoc. Biol. 57: 168–173; 1995.
Time course of coronary vascular endothelial adhesion molecule expression during reperfusion of the ischemic feline myocardium
Authors: Weyrich Andrew S , Buerke Michael , Albertine Kurt H , Lefer Allan M 
Published: January 2018

Abstract
The time course of endothelial P-selectin, ICAM-1, and E-selectin expression was studied in a feline model of myocardial ischemia and reperfusion. Cats were subjected to 90 min of myocardial ischemia followed by 0, 10, 20, 60, 150, or 270 min of reperfusion. At the end of reperfusion, the coronary vasculature was examined immunohistochemically to localize monoclonal antibodies (mAbs) PB1.3, RR1/1, and Cyl787 directed against P-selectin, ICAM-1, and E-selectin, respectively. Immuno-histochemical localization for P-selectin, recognized by mAb PB1.3, was maximally expressed 20 min after reperfusion in 60 ± 6% of coronary venules (P &lt; 0.05 compared to non-reperfused controls), and covered 59 ± 3% of the endothelial cell perimeter of immunostained coronary venules. Immunolocalization of mAb PB1.3 gradually declined at 60, 150, and 270 min of reperfusion. Immunohistochemical localization of mAb RR1/1 (anti-ICAM-1) in endothelial cells of coronary venules was observed to a modest extent in non-ischemic myocardium and at 10, 20, and 60 min of reperfusion, but was significantly increased following 150 and 270 min of reperfusion (P &lt; 0.05 compared non-reperfused controls). At 270 min post-reperfusion, mAb RR1/1 was seen in 50 ± 4% of coronary venules. Endothelial immunolocalization of mAb Cyl787 (anti-E-selectin) was only observed in 13 ± 1 and 14 ± 3% of coronary venules after 150 and 270 min of reperfusion, respectively, suggesting that pronounced expression of E-selectin does not occur within 270 min after reperfusion. These results demonstrate sequential expression of three major endothelial cell adherence molecules in situ following myocardial ischemia and reperfusion. The timing of endothelial cell expressed P-selectin and ICAM-1 could coordinate neutrophil trafficking during the early stages of reperfusion. J. Leukoc. Biol. 57: 45–55; 1995.
In vivo activation of heterophil function in chickens following injection with Salmonella enteritidis-immune lymphokines
Authors: Kogut Michael H , McGruder Edward D , Hargis Billy M , Corner Donald E , DeLoach John R 
Published: January 2018

Abstract
We have previously shown that increased resistance to Salmonella enteritidis organ infectivity in day-old chicks was conferred by the immunoprophylactic administration of S. enteritidis-immunc lymphokines (ILK). This resistance was associated with a significant increase in the number of circulating heterophils 4 h after ILK injection. The objective of the present study was to evaluate heterophil function following the administration of ILK in day-old chicks. Significant increases (P &lt; 0.001) in adherence, chemotaxis, and phagocytosis of S. enteritidis were found with heterophils isolated from ILK-injected chickens compared to the heterophils isolated from birds injected with either pyrogen-free saline or lymphokines from non-immune T cells. After phagocytosis, the heterophils from the ILK-injected chickens were also able to kill significantly greater numbers of S. enteritidis more rapidly than did the heterophils from the saline-injected control birds (within 30 min, control cells killed 21.89% of the bacteria whereas ILK-treated cells killed 88.22%). We also found that the heterophils from the ILK-injected birds were more efficient killers of S. typhimurium, S. gallinarum, and E. coli These results strongly suggest that the protection against S. enteritidis organ invasion induced by the prophylactic treatment of day-old chicks with ILK involves activated heterophils which migrate rapidly to the inflammatory stimulus where they phagocytize and kill the bacteria. J. Leukoc. Biol. 57: 56–62; 1995.
Signal transduction by cell adhesion receptors in leukocytes
Authors: Rosales Carlos , Juliano Rudy L 
Published: January 2018

Abstract
Leukocytes usually pass through the blood stream as nonadherent cells, but during an immune response and inflammation, they become adherent in order to migrate through tissues. Three families of adhesion molecules, the immunoglobulin family, the selectins, and the integrins, participate in interactions between leukocytes and tissues. Near sites of inflammation, leukocytes initially interact with the endothelium via selectins, causing them to slow down and to roll along the walls of blood vessels. Next, chemoattractans induce the activation of integrins on leukocytes. Finally, activated integrins mediate leukocyte migration through the endothelium into the inflamed site. Interactions of leukocytes with other cells and various extracellular matrix (ECM) proteins lead to different functional cell responses, including changes in growth, behavior, and differentiation. Many of these interactions are mediated by integrins, which “integrate” ECM protein signals with the cytoskeleton and which also act as true receptors that generate biochemical signals within the cell. Changes in pH, cytoplasmic Ca2+ concentration, phosphorylation, and gene induction have all been observed after integrin engagement. Adhesion-mediated gene induction in monocytes is perhaps the best example that integrins initiate signaling cascades in the cell to deliver information from the ECM all the way to the nucleus. J. Leukoc. Biol. 57: 189–198: 1995.
Distinct biochemical responses of hepatic macrophages and endothelial cells to platelet-activating factor during endotoxemia
Authors: Gardner Carol R , Laskin Jeffrey D , Laskin Debra L 
Published: January 2018

Abstract
Acute endotoxemia is associated with activation of hepatic macrophages and endothelial cells. These cells release a variety of inflammatory mediators that have been implicated in tissue injury. In the present studies, we analyzed the biochemical responses of these cells to platelet-activating factor (PAF), a lipid autacoid released during hepatic inflammatory responses. To induce acute endotoxemia, rats were injected intravenously with lipopolysaccharide (LPS). Using the calcium sensitive fluorescent indicator dye Indo-1, we found that PAF induced a rapid and transient increase in intracellular calcium in both hepatic macrophages and endothelial cells. Induction of acute endotoxemia resulted in an increase in the amount of calcium mobilized by both cell types. Although endothelial cells from control rats were less responsive to PAF than macrophages, these cells were more sensitive to in vivo endotoxin. PAF was also found to cause a rapid decrease in intracellular pH in hepatic macrophages that was quantified by fluorescence image analysis using the pH sensitive dye SNAFL-calcein. This decrease occurred more rapidly in macrophages from endotoxemic rats. In cells from both control and endotoxemic rats, the effects of PAF on intracellular pH were inhibited by the specific PAF antagonist triazolam. In contrast to hepatic macrophages, PAF had no effect on intracellular pH in endothelial cells from either control or endotoxemic rats. Ligand binding studies demonstrated that both hepatic macrophages and endothelial cells possess high affinity binding sites for PAF. Macrophages expressed 6- to 7-fold more binding sites/cell than endothelial cells and exhibited a higher Kd. Whereas treatment of rats with LPS had no effect on the Kd for PAF binding to macrophages or on the number of binding sites, a significant increase in both of these receptor characteristics was observed in endothelial cells. Taken together, the present data suggest that the biochemical responses of endothelial cells and macrophages to PAF are distinct. Furthermore, cellular activation induced by PAF in endothelial cells appears to be independent of changes in intracellular pH. J. Leukoc. Biol. 57: 269–274; 1995.
Differential effects of anti-inflammatory cytokines (IL-4, IL-10 and IL-13) on tumoricidal and chemotactic properties of human monocytes induced by monocyte chemotactic and activating factor
Authors: Yano Seiji , Sone Saburo , Nishioka Yasuhiko , Mukaida Naofumi , Matsushima Kouji , Ogura Takeshi 
Published: January 2018

Abstract
The effect of recombinant human IL-4, IL-10, and IL-13 on the chemotaxis and antitumor activity of human blood monocytes induced by monocyte chemotactic and activating factor (MCAF) was examined. MCAF alone did not induce monocyte-mediated cytotoxicity against human melanoma (A375-M) cells whereas it significantly enhanced the cytotoxicity by norMDP-stimulated monocytes. MCAF, unlike IFN-γ, had no priming effect on monocyte activation by norMDP. MCAF acted with norMDP or LPS to enhance the production of both IL-1β and TNF-α. Enhanced cytotoxicity of monocytes stimulated with MCAF plus norMDP was reduced by IL-1 receptor antagonist and anti-TNF-α antibody. IL-4, IL-10, and IL-13 suppressed the generation of antitumor activity and cytokine production (IL-1β and TNF-α) of monocytes stimulated with MCAF plus norMDP or LPS. Chemotaxis of monocytes induced by MCAF was not affected by norMDP or any of the anti-inflammatory cytokines (IL-4, IL-10, and IL-13). Moreover, the pretreatment of monocytes with anti-inflammatory cytokines did not suppress monocyte-chemotaxis. These findings suggest that in vivo recruitment and anti-tumor expression of blood monocytes induced by MCAF may be differently regulated by anti-inflammatory cytokines in vivo. J. Leukoc. Biol. 57: 303–309; 1995.