bluuebunny/crossref_metadata_2025_split huggingface dataset:
Monoclonal antibody EG2 reactivity cannot be used as an immunohistochemical activation marker for eosinophils
Authors: Jahnsen Frode L , Brandtzaeg Per 
Published: January 2018

Abstract
To the Editor: Rosenberg and Tiffany recently described [1] that the presumed “activation-specific” antibody EG2 recognized only one (the smallest) of three glycosylated forms (18 kDa, 20 kDa, and 22 kDa) of eosinophil cationic protein (ECP). On the basis of this finding they proposed two alternative ways to explain how the epitope for EG2 was accessible only in activated eosinophils. They suggested that deglycosylation of ECP could occur in conjunction with activation and secretion; this was unlikely though because the 18-kDa form constitutes a substantial fraction of ECP (by Western blotting) even in resting eosinophils [1, 2]. Then they speculated that the 18-kDa form of ECP might be functionally undetectable prior to secretion.1 We have recently shown, however, that cellular EG2 reactivity does not reliably discriminate between resting and activated eosinophils by immunocytochemistry and immunohistochemistry [3]. All blood eosinophils from healthy individuals were strongly EG2-positive when fixed in formalin, and a substantial fraction reacted in the unfixed or acetone-fixed state as well, although with variable intensity. Even after maximum activation (phorbol ester) EG2 could not discriminate eosinophils from their resting counterparts [4].
Monoclonal antibody EG2 reactivity: the need for clarification
Authors: Jahnsen Frode L , Brandtzaeg Per 
Published: January 2018

Abstract
A final comment: We regret that Rosenberg and Tiffany in their response (1) apparently considered our letter (2) about immunohistochemical reactivity of the monoclonal antibody EG2 as criticism of their excellent work (3). Our intention was simply to help explain their biochemical findings in terms of immunocytochemical and immunohistochemical staining performance of EG2 in the light of recent information (4).
Induction of macrophage binding to virally infected cells by low levels of lipopolysaccharide
Authors: Derrick Steven C , LeBlanc Paul A 
Published: January 2018

Abstract
Bone marrow culture-derived macrophages (BMCM) and vesicular stomatitis virus-infected BALB/e-3T3 cells (3T3-VSV) were used to determine whether macrophages could be activated to bind virally infccted cells. Although lipopolysaccharide (LPS)-activated BMCM bound some uninfected BALB/c-3T3 cells, the number of targets that were bound increased with increasing times between infection and assay. Fur thermore, LPS-activated BMCM bound more 3T3-VSV cells than did control macrophages. As more targets were added, the number of targets bound by the unactivated macrophagcs remained relatively level. However, the number of targets bound by the activated macrophages increased with increasing concentrations of added targets until they reached a plateau that was eight times greater than that bound by the unactivated BMCM. When BMCM were exposed to LPS for 24 h before assay, they lost both their ability to bind to 3T3-VSV and their cyto lytic activity against those targets. However, as when using P815, a standard tumor target, the acquisition of binding of 3T3-VSV could be separated from macrophage cytolytic activity against those targets. The amount of LPS required to activated BMCM for increased binding of 3T3-VSV cells was 10–100 times lower than that needed to induce cytolytic activity for 3T3-VSV cells. Each of these values was approximately 100-fold lower than the amount of LPS required to induce the corresponding ac tivity (binding or cytotoxicity) by using P815 targets. J. Lcukoc. Biol 57: 569–573; 1995.
Intracellular multiplication of Legionella pneumophila in HL-60 cells functionally differentiated in response to 22-oxacalcitriol
Authors: Matsuzaki Miwako , Shimamoto Yoshinori , Watanabe Masayuki , Kukita Akiko , Yoshida Shin-ichi , Tadano Jutaro 
Published: January 2018

Abstract
The agent 1,25-dihydroxy vitamin D3 (D3) induces the differentiation of HL-60 human leukemia cells into functional monocyte-like cells that can support the intracellular multiplication of Legionella pneumophila. 22-Oxacalcitriol (OCT), a synthetic analogue of D3, ex hibits greater differentiation-inducing activity than D3 in WEHI-3 mouse leukemia cells and has been suggested to be clinically more useful because of its lower hypercalcemic activity. The abilities of OCT and D3 to induce the functional differentiation of human leukemia HL-60 cells have now been investigated. OCT induced the differentiation of HL-60 cells into monocyte-like cells to a similar extent as D3. Thus, both OCT and D3 increased (1) the surface expression of CD11b, CD11c, CD14, and CD35; (2) nonspecific esterase staining; and (3) phagocytic ac tivity toward fluorescent beads. HL-60 cells differentiated in response to OCT also supported the intracellular mul tiplication of L. pneumophila. Activation of both OCT-and D3-treated HL-60 cells with human recombinant interferon-γ (IFN-γ) for 24 h before infection markedly inhibited L. pneumophila multiplication. IFN-γ activation enhanced superoxide anion generation by D3-treated HL-60 cells but not by OCT-treated HL-60 cells, suggesting that the inhibition of L. pneumophila multiplication in IFN-γ-activated cells is independent of superoxide generation. Finally, D3, but not OCT, markedly stimu lated the formation of osteoclast-like multinudeated cells from mouse bone marrow cells, consistent with the lower hypercalcemic activity of OCT. J. Leukoc. Biol. 57: 574–580; 1995.
Effects of endotoxin on expression of VLA integrins by human bronchoalveolar lavage macrophages
Authors: Kang Yuan-Hsu , Lee Che-Hung , Brummel Sara E , Newball Harold H , Forrester Joe 
Published: January 2018

Abstract
Endotoxin (lipopolysaccharide, LPS) is known to induce inflammatory responses, such as mono cyte/macrophage adherence, migration, and accumulation. Recruitment and accumulation of macrophages during infection and inflammation are regulated by integrin-mediated cell-extracellular matrix interactions. In the present report, we studied the effects of LPS on the expression of VLA-5 (α 5 β 1), VLA-3 (α 3 β 1), and VLA-2 (α 2 β 1 ) integrins and fibronectin (FN) by human alveolar macrophages in an attempt to understand the mechanism by which LPS regulates macrophage adhesion to matrix proteins. Bronchoalveolar lavage macrophages were treated with varying concentrations of Escherichia coli LPS for different times and evaluated for expression of the integrins and FN by immunofluorescence, immunoelectron microscopy, autoradiography, and radioim munoassay. Immunofluorescent and immunoelectron microscopic observations showed that VLA integrins were constitutively expressed on the cell surface and con centrated on the microvilli and pseudopodia of the mac rophages. The effects of LPS on expression of the inte grins were dose and time related. VLA-5 expression was increased after 30 min of stimulation by LPS, suggesting that LPS may induce rapid secretion of the integrin. However, incubations with LPS longer than 30 min decreased VLA-5 expression in a dose-dependent pattern. LPS also caused dose-related decreases in the expression of VLA-3 and VLA-2 integrins and increases of intracel lular FN 24 h after stimulation. The results suggest that a prolonged exposure to LPS may impede VLA inte grin-mediated migration and result in local accumulation of macrophages in the lung. J. Leukoc. Biol. 57: 624–634; 1995.
Immune complexes increase nitric oxide production by interferon-γ-stimulated murine macrophage-like J774.16 cells
Authors: Mozaffarian Neelufar , Berman Joan W , Casadevall Arturo 
Published: January 2018

Abstract
Murine macrophage-like J774.16 cells were tested for changes in nitric oxide production upon incu bation with immune complexes. Cryptococcus neoformans capsular polysaccharide and polysaccharidespecific monoclonal antibodies were added to J774.16 cells in the presence and absence of recombinant murine interferon-γ (IFN-γ). The effect of immune complexes on nitrite synthesis was both concentration dependent and isotype dependent. In the presence of IFN-γ, immune complexes of IgGl, IgG2a, IgG2b, or IgG3 isotype in creased nitrite levels, whereas complexes of IgM isotype did not. Immune complexes did not alter nitrite production by unstimulated macrophages. Antibody alone, anti gen alone, and antigen with irrelevant IgGl antibody did not augment nitrite formation, either in the presence or absence of IFN-γ. indicating a requirement for FCγR cross-linking. These results suggest that IgG isotypes may offer additional protection against pathogens by enhancing macrophage nitric oxide production, J. Lcukoc. Biol. 57: 657–662; 1995.
Thrombopoietin, the c-mpl ligand, is a major regulator of platelet production
Authors: Broudy Virginia C , Kaushansky Kenneth 
Published: January 2018

Abstract
Hematopoiesis is regulated by a family of glycoproteins, the hematopoietic growth factors. Although the cytokines that influence the late stages of granulopoiesis (granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor) or erythropoiesis (erythropoietin) have been identified, characterized, and cloned, and have been in clinical use since that late 1980’s, the cytokine that stimulates thrombopoiesis had remained elusive. By using strategies based on the c-mpl receptor, several groups have recently succeeded in purifying and cloning thrombopoietin [1–6]. This study outlines the cloning and biological characterization in vitro and in vivo of thrombopoietin, a major regulator of platelet production. J. Leukoc. Biol. 57: 719–725; 1995.
Cytokine production profile of early thymocytes and the characterization of a new class of chemokine
Authors: Kelner Gregory S , Zlotnik Albert 
Published: January 2018

Abstract
By using a variety of molecular techniques, we have characterized the cytokine profile of pro-T cells. During this characterization we cloned a novel cytokine that has chemotactic activities. We have designated this cytokine lymphotactin. The structural analysis, chromosomal location, and biological properties of lymphotactin provide strong evidence that this cytokine represents a new class of chemokine. J. Leukoc. Biol. 57: 778–781; 1995.
Receptors, signal transduction, and spectrum of action of monocyte chemotactic protein-1 and related chemokines
Authors: Sozzani Silvano , Locati Massimo , Zhou Dan , Rieppi Monica , Luini Walter , Lamorte Giuseppe , Bianchi Giancario , Polentarutti Nadia , Allavena Paola , Mantovani Alberto 
Published: January 2018

Abstract
Chemokines are a bipartite family of chemotactic proteins that bear the structural hallmark of four cysteine residues, the first two of which are in tandem. The spectrum of action of C-C chemokines, monocyte chemotactic protein-1 (MCP-1), MCP-2, and MCP-3, in particular, encompasses, in addition to monocytes, other leukocyte populations. Evidence is presented that MCP-1, MCP-2, and MCP-3 are active on natural killer cells. Available information on receptor usage by MCP-1 and related chemokines and signal transduction pathways is reviewed. A better understanding of signaling mechanisms will provide a new basis for therapeutic strategies. J. Leukoc. Biol. 57: 788–794; 1995.
Neutrophils are essential for resolution of primary and secondary infection with Listeria monocytogenes
Authors: Rakhmilevich Alexander L 
Published: January 2018

Abstract
The role for neutrophils in the resolution of primary and secondary infection with Listeria monocytogenes was studied. The results show that although control mice started to clear Listeria from their spleens and livers between days 2 and 4 of sublethal primary infection and eradicated bacteria in 2 weeks, mice given a specific granulocyte-depleting antibody (RB6-8C5) on days 4 or 6 of infection developed lethal listeriosis. Likewise, treatment of immunized mice with RB6-8C5 monoclonal antibody abolished their acquired ability to resolve a lethal challenge infection. The results demonstrate that neutrophils are necessary for the resolution of secondary and primary Listeria infection. J. Leukoc. Biol. 57: 827–831; 1995.
Slow Ca2+ waves in large myeloid cells as a result of a diffusible cytosolic factor
Authors: Roberts G M , Davies E V , Hallett M B 
Published: January 2018

Abstract
In the work reported here evidence is provided that shows the slow wave of Ca2+ large neonatal myeloid cells provoked by formyl-Met-Leu-Phe was generated by spatially delayed Ca2+ influx. Evidence is provided that the delay in Ca2+ influx was the result of diffusion of a factor from the Ca2+ storage site, which is responsible for Ca2+ channel opening. The location of the Ca2+ release site was correlated with a region near the nucleus, probably a specialized region of endoplasmic reticulum. It is proposed that similar mechanisms of Ca2+ signaling occur in mature myeloid cells, such as neutrophils, but on a shorter time scale as a consequence of their smaller size. J. Leukoc. Biol. 57: 837–841; 1995.
Profile of immunoglobulin heavy chain variable gene repertoires and highly selective detection of malignant clonotypes in acute lymphoblastic leukemia
Authors: Greenberg Steven J , Choi Youngnim , Ballow Mark , Du Tian-Long , Ward Pamela M , Rickert Michael H , Frankel Stanley , Bernstein Steven H , Brecher Martin L 
Published: January 2018

Abstract
The predominant B cell immunoglobulin heavy chain variable gene (IgH-V) usage and the uniquely rearranged, clonotype-specific variable-diversity-joining region gene (VDJ) sequences were identified in patients with B cell acute lymphoblastic leukemia (B-ALL) using a novel DNA-based gene amplification strategy. The approach allows a thorough and sensitive determination of the number of clonal leukemic IgH rearrangements and their precise V gene usage. This strategy may be applied in the detection of minimal residual disease, in surveillance after induction of disease-free states, and in analyzing the effectiveness of purging autologous bone marrow of malignant clones. An initial primary polymerase chain reaction (PCR), directed by an IgH-J generic primer and a complement of family-specific IgH-V primers, defined the major B cell IgH-V gene usage. Use of an IgH-J generic primer supplanted the use of a constant region primer anchor and thus eliminated the need to target mRNA by the traditional RNA reverse transcription–PCR amplification method. Monoclonality of rearranged VDJ bands was further substantiated by high-resolution denaturant gel electrophoretic analysis. The predominant amplified bands were subcloned and sequenced. By sequencing through VDJ juxtaposed regions, that is, the third complementarity-determining region, clonotype-specific primers were developed and used in a secondary clonotype primer-directed PCR (CPD-PCR) to detect, with extreme sensitivity and specificity, a unique B cell clone. Analysis of the products of the CPD-PCR permitted the detection of a single malignant cell among 1 million polyclonal cells and superseded the constraints of prior studies that have provided a limited evaluation of family variable gene repertoire usage. Leukemic clonal rearrangements were detected in 100% of the eight cases of pediatric and two cases of adult B-ALL studied. Two or more clonal IgH-VDJ amplified sequences were observed in 50% of the B-ALL bone marrows analyzed. In two cases, clonotype-specific oligodeoxynucleotide primers, derived from B-ALL VDJ sequences, directed the secondary CPD-PCR, and disease activity was monitored after chemotherapy and allogeneic bone marrow transplantation. J. Leukoc. Biol. 57: 856–864; 1995.
Poxvirus-based vaccine candidates for cancer, AIDS, and other infectious diseases
Authors: Perkvs Marion E , Tartaglia James , Paoletti Enzo 
Published: January 2018

Abstract
Over the past 12 years, the poxvirus vector technology has provided scientists with valuable reagents to achieve high-level expression of proteins, to address questions of structure-function relationship of specific polypeptides, to investigate the immunobiology of specific pathogens, and to develop recombinant vaccine candidates. It is this last role that has drawn enthusiasm from the medical community because of the potential this technology has to provide novel approaches for addressing urgent needs in human and veterinary medicine. From one perspective, the safety issues surrounding the use of vaccinia-based vaccine candidates have been addressed with the development of the NYVAC and ALVAC vectors. Evaluation of these novel poxvirus vectors are in progress to determine their potential impact on cancer and infectious disease. J. Leukoc. Biol. 58: 1–13; 1995.
Binding of Gc globulin (vitamin D binding protein) to C5a or C5a des Arg is not necessary for co-chemotactic activity
Authors: Kew Richard R , Mollison Karl W , Webster Robert O 
Published: January 2018

Abstract
Gc globulin (vitamin D binding protein) has been shown to augment significantly die leukocyte chemotactic activity of the activated complement peptides C5a and C5a des Arg. However, the mechanism of chemotaxis enhancement is not known. Natural C5-derived peptides contain a carbohydrate side chain that comprises approximately 25% of the mass of the 11-kDa peptides. Previous studies have demonstrated that Gc globulin binds to C5-derived peptides via sialic acid residues on this carbohydrate side chain. The necessity of this carbohydrate side chain for chemotaxis enhancement by Gc globulin was investigated by using both natural (glycosylated) and recombinant (carbohydrate-free) peptides. The dose-response curves of neutrophil chemotaxis to recombinant C5a or C5a des Arg plus Gc globulin were identical to those observed with the naturally derived peptides, despite the fact that natural C5a bound to Gc globulin while the recombinant C5a failed to bind this protein. Moreover, neutrophils pretreated with Gc globulin then washed before addition to the chemotaxis assay displayed significantly enhanced movement to C5a alone. These results indicate that the binding of C5a/C5a des Arg to Gc globulin is not necessary for their chemotactic activity to be augmented. Furthermore, these results demonstrate that the co-chemotactic activity of Gc globulin is generated on the cell surface, independent of C5a binding to its receptor. J. Leuhoc. Biol. 58: 55–58; 1995.
Murine Th1 and Th2 cell clones differentially regulate macrophage nitric oxide production
Authors: Taub Dennis D , Cox George W 
Published: January 2018

Abstract
Previous studies have demonstrated that the combination of the T helper cell 1 (Thl)-derived cytokines interleukin (IL)-2 and interferon (IFN)-γ induces nitric oxide (NO) production and tumor cytolysis by mouse peritoneal macrophages and the mouse macrophage cell line ANA-1 in vitro. Conversely, the Th2-derived cytokine IL-4 inhibits IL-2 and IFN-γ-induced NO production and tumor cytolysis by ANA-1 macrophages. To examine the paracrine regulatory effects of Thl and Th2 cells on macrophages, various mouse T cell clones were tested for their ability to regulate NO production by mouse peritoneal macrophages or ANA-1 macrophages. Antigen, superantigen, and mitogen stimulated Th1 cells but not Th2 cells induced NO production by macrophages. Supernatants from these activated Th1 clones also induced NO production by peritoneal macrophages and ANA-1 macrophages. Neutralization analysis using monoclonal anticytokine antibodies revealed that both IL-2 and IFN-γ production by activated Th1 cells were required for the production of NO by macrophages. Co-culture studies using a panel of Th2 cell clones that share the same antigen specificity revealed that these cells suppressed Th1-mediated macrophage activation. The Th2-mediated impairment of Th1-induced NO production was primarily due to the secretion of IL-4. IL-4 appeared to have a direct effect on macrophage activation because neither mitogen-induced proliferation of Th1 cells nor cytokine production by Th1 cells were affected by IL-4. Overall, these results suggest that a potent paracrine regulatory network involving Th1 cells and Th2 cells may control the activation of macrophages for NO production and antitumor cytotoxicity. J. Leukoc. Biol. 58: 80—89; 1995.
Gamma/delta T lymphocytes in viral Infections
Authors: Wallace Marianne , Malkovsky Miroslav , Carding Simon R 
Published: January 2018

Abstract
T lymphocyte progenitors differentiate into two distinct T cell lineages. Although the αβ and γδ T cell lineages resemble each other phenotypically and functionally, there are some striking differences. Some γδ T cells recognize, similarly to αβ T cells, peptides presented by major histocompatibility complex (MHC) proteins or MHC-like molecules. However, there are γδ T cells that recognize MHC molecules in a fundamentally different manner in comparison with αβ T cells. Also in contrast to aLβ T lymphocytes, many γδ T cells are capable of recognizing nonpeptide antigens. Most responses of γδ T cells appear to be directed against microbial pathogenic agents including bacteria, parasites, and viruses. In particular, the potent cytotoxic responses of γδ T cells against cells infected with, for example, herpesviruses or lentiviruses may be essential for the overall antiviral defense of vertebrates. The analysis of antiviral immunosurveillance by γδ T cells is crucial for understanding the unique biological role of this lymphocyte subset.
Costimulation of CD4+ and CD8+ T cells through CD26: The ADA-binding epitope is not essential for complete signaling
Authors: De Meester Ingrid A , Kostens Luc L , Vanham Guido L , Vanhoof Greet C , Vingerhoets Johan H , Gigase Paul L , Scharpé Simon L 
Published: January 2018

Abstract
It was previously shown that CD26 (DPP IV, EC 3.4.14.5) is a binding site for adenosine deaminase (ADA, EC 3.5.4.4) on T cells and that costimulation by some anti-CD26 monoclonal antibodies (mAbs) and anti-CD3 induces CD4+ T cell proliferation. The CD26 epitopes involved in costimulation, the precise sequence of the events preceding proliferation, and the response of CD8+ compared with CD4+ T cells to CD26 were not extensively studied. We therefore compared the effects of the novel TA5.9 anti-CD26 mAb, recognizing an ADA-binding epitope, and the clearly distinct anti-Ta1 reference anti-CD26 mAb for their costimulatory properties in various T cell subsets. Both purified CD4+ and CD8+ T cells proliferated upon costimulation with anti-CD3 and either anti-CD26 mAb, but anti-TA5.9 mAb induced a more potent response than anti-Tal. Either anti-CD26 mAb, together with anti-CD3, caused a similar sequential up-regulation of CD69, CD25 (IL-2Rα), and CD71 (transferrin receptor) expression on CD4+ and CD8+ T cells. The activation markers appeared faster on the CD45R0+ than on the CD45R0− subsets. After costimulation, CD4+ T cell cultures contained significant amounts of the Th1 cytokines EL-2, interferon-γ (IFN-γ), and tumor necrosis factor-α (TNF-α). In CD8+ T cell cultures relatively more IFN-γ and TNF-α but almost no IL-2 was measured after triggering of CD3 and CD26. Our data demonstrate that the recognition of the ADA-binding epitope is not a prerequisite for the costimulatory capacity of anti-CD26 mAbs. Both CD4+ and CD8+ T cells and their CD45R0−and CD45R0+ subsets are sensitive to various aspects of activation via CD26, but the magnitude and/or kinetics differ according to the anti-CD26 used and the T cell subset studied.