bluuebunny/crossref_metadata_2025_split huggingface dataset:
Monoclonal antibodies to the common γ-chain as cytokine receptor antagonists in vivo: effect on intrathymic and intestinal intraepithelial T lymphocyte development
Authors: Malek Thomas R , Levy Robert B , Adkins Becky , He You-Wen 
Published: January 2018

Abstract
Mice lacking a functional γc subunit of cytokine receptors exhibit profound defects in the development of multiple lymphoid lineages. To investigate the role of γc-dependent cytokines in T cell development, the phenotype of developing T cells was compared in interleukin (IL)-7Rα-deficient mice and anti-γc mAb-treated chimeric mice reconstituted with adult bone marrow cells or subsets of pro-T cells. These studies indicate that γc contributes to T cell development at multiple stages of pro-T cell maturation and that IL-7/IL-7R is the primary cytokine for thymic-dependent T cell development. However, our data also implicate other γc-dependent cytokines during thymic T cell development. By contrast, substantial intestinal intraepithelial lymphocytes (IEL) development was observed in the intestinal intraepithelium in both types of mice. Analysis of IL-7Rα-deficient mice indicates that the IL-7/IL-7R system is critical only for the development of TCR γδ+ IEL. However, the inhibitory activity of the anti-γc mAb in the chimeric mouse model suggests that additional γc-utilizing cytokines regulate the development of the remaining subsets of IEL.
Superoxide production by phagocytosing macrophages in relation to the intracellular distribution of oxygen
Authors: James Philip E , Grinberg Oleg Y , Swartz Harold M 
Published: January 2018

Abstract
We simultaneously measured the concentration of oxygen ([O2]) within the phagosomal and extracellular compartments of macrophages. By combining electron paramagnetic resonance (EPR) oximetry techniques with that of spin-trapping, we found that a significant difference in oxygen concentration ([O2]) exists between these two compartments and we were able to monitor (1) how [O2] in the extracellular compartment and the rate of mitochondrial consumption affected this difference in [O2], and (2) to what extent this gradient of [O2] influenced production of reactive oxygen species by phagosomes. Under conditions where the [O2] in the inflowing gas was high (210 μM; air), the [O2] in the extracellular and phagosomal compartments was 180 and 141 μM, respectively. This was sufficient to maintain maximum superoxide production in these cells. When extracellular [O2] was reduced to 84 or 36 μM, the [O2] in phagosomes within the cells (31.7 and 7.7 μM, respectively) was too low to maintain superoxide production by the NADPH-oxidase system within the phagosomes. The [O2] in the extracellular compartments of these samples, however, was always sufficient to maintain superoxide production by phagosomes at the cell surface. Our findings suggest that the distribution of oxygen surrounding and within macrophages can influence their ability to perform microbicidal and tumoricidal functions, even at an [O2] in the media that appears to be adequate. J. Leukoc. Biol. 64: 78–84; 1998.
Resident mast cells are important for eotaxin-induced eosinophil accumulation in vivo
Authors: Das Anuk M , Flower Roderick J , Perretti Mauro 
Published: January 2018

Abstract
Eotaxin administration intraperitoneally, but not into dorsal air-pouches, of ovalbumin-sensitized mice exhibiting blood eosinophilia induced a threefold increase in eosinophil (Eφs) infiltration. Transfer of 1 × 106 mixed peritoneal cavity cells (PCC), containing 3.5 to 4.5 × 104 mast cells (MC), from donor mice to air-pouches of sensitized (but not unsensitized) recipient mice, established an Eφ infiltration to eotaxin (vehicle, 0.86 ± 0.27 × 106; eotaxin, 1.63 ± 0.16 × 106 Eφs/air-pouch). Neutrophil numbers were also increased. When MC-depleted (−93%) PCC were injected into air-pouches of recipient animals, Eφ infiltration was not supported (−52%). Injection of macrophage-depleted (−99%) PCC into air-pouches elicited a full Eφ response to eotaxin but not neutrophil infiltration (−81%). Systemic dexamethasone treatment of recipient mice reduced Eφ accumulation; treatment of donor mice only reduced neutrophil accumulation. Our study points to a crucial role for MC in Eφ recruitment by eotaxin. J. Leukoc. Biol. 64: 156162; 1998.
In vivo regulation of PECAM-1 activity during acute endothelial dysfunction in the rat mesenteric microvasculature
Authors: Scalia Rosario , Lefer Allan M 
Published: January 2018

Abstract
The relationship between acute endothelial dysfunction and the extravasation of leukocytes was studied in vivo with intravital microscopy of the rat mesenteric microvasculature. Acute endothelial dysfunction of the rat mesenteric microvasculature was induced in vivo by superfusing the mesentery for 90 min with one of three different stimulating agents: NG-nitro-L-arginine methyl ester (l-NAME, 50 μM), thrombin (0.5 U/mL), or hydrogen peroxide (H2O2, 50 μM). All three agents induced a similar increase in leukocyte rolling and adherence, which was significantly greater than that observed in control rats superfused with Krebs-Henseleit solution (P &lt; 0.01). Transendothelial migration of leukocytes into the perivascular space was also increased by superfusion with l-NAME, thrombin, or H2O2. However, there was a greater increase in the number of migrated leukocytes in the rat mesentery after l-NAME and H2O2 superfusion than that observed during thrombin superfusion. In vivo infusion of a neutralizing antibody against platelet-endothelial cell adhesion molecule-1 (PECAM-1) specifically inhibited l-NAME-induced and H2O2-induced migration of leukocytes but did not prevent extravasation of leukocytes induced by thrombin. In rat mesenteries superfused with the three different stimuli, immunohistochemical analysis of endothelial cell adhesion molecules expressed on the microvascular endothelium revealed a significant increase of ICAM-1, but not PECAM-1, endothelial cell surface expression (P &lt; 0.01 and P &gt; 0.05 vs. control rats, respectively). Our data confirm a key role for PECAM-1 acutely in leukocyte extravasation in vivo and indicate that the involvement of constitutively expressed PECAM-1 in leukocyte transendothelial migration is preferentially correlated to oxidative stress-related stimuli in the microvascular endothelium. J. Leukoc. Biol. 64: 163–169; 1998.
HIV load in highly purified CD8+ T cells retrieved from pulmonary and blood compartments
Authors: Semenzato Gianpietro , Agostini Carlo , Chieco-Bianchi Luigi , De Rossi Anita 
Published: January 2018

Abstract
The pulmonary microenvironment can be HIV infected from the asymptomatic period of HIV infection and it has been demonstrated that HIV presence elicits a discrete virus-specific CTL immune response in the lungs. In this study we analyzed T cell subsets and compared the proportion of CD8+ T cells harboring HIV in the lung and in the circulation of HIV-seropositive patients with T cell alveolitis. Proviral load was assessed using the DNA-polymerase chain reaction technique on highly purified CD8+ T cells isolated from peripheral blood and bronchoalveolar lavage. The proviral load of pulmonary CD8+ T cells showed an upward trend with respect to corresponding samples isolated from the peripheral blood of the same patients. J. Leukoc. Biol. 64: 298–301; 1998.
TNF and IL-6 mediate MIP-1α expression in bleomycin-induced lung injury
Authors: Smith Robert E , Strieter Robert M , Phan Sem H , Lukacs Nicholas , Kunkel Steven L 
Published: January 2018

Abstract
Previously, macrophage inflammatory protein-1α (MIP-1α), a member of the C-C chemokine family, has been implicated in bleomycin-induced pulmonary fibrosis, a model of the human disease idiopathic pulmonary fibrosis. Neutralization of MIP-1α protein with anti-MIP-1α antibodies significantly attenuated both mononuclear phagocyte recruitment and pulmonary fibrosis in bleomycin-challenged CBA/J mice. However, the specific stimuli for MIP-1α expression in the bleomycin-induced lesion have not been characterized. In this report, two mediators of the inflammatory response to bleomycin, tumor necrosis factor (TNF) and interleukin-6 (IL-6), were evaluated as putative stimuli for MIP-1α expression after bleomycin challenge in CBA/J mice. Elevated levels of bioactive TNF and IL-6 were detected in bronchoalveolar lavage (BAL) fluid and lung homogenates from bleomycin-treated CBA/J mice at time points post-bleomycin challenge, which precede MIP-1α protein expression. Treatment of bleomycin-challenged mice with soluble TNF receptor (sTNFr) or anti-IL-6 antibodies significantly decreased MIP-1α protein expression in the lungs. Furthermore, normal alveolar macrophages secreted elevated levels of MIP-1α protein in response to treatment with TNF plus IL-6 or bleomycin plus IL-6, but not TNF, bleomycin, or IL-6 alone. Finally, leukocytes recovered from the BAL fluid of bleomycin-challenged mice secreted higher levels of MIP-1α protein, compared to controls, when treated with TNF alone. Based on the data presented here, we propose that TNF and IL-6 are part of a cytokine network that modulates MIP-1α protein expression in the profibrotic inflammatory lesion during the response to intratracheal bleomycin challenge. J. Leukoc. Biol. 64: 528–536; 1998.
The significance of zinc for leukocyte biology
Authors: Wellinghausen Nele , Rink Lothar 
Published: January 2018

Abstract
Zinc is an essential element important for growth, the nervous system, and especially the immune system. Zinc deficiency as well as levels well above normal, due to high-dose treatment, showed an impaired immune function. This review summarizes the current status of zinc's significance for leukocyte biology and health. In detail, the physiology of zinc and the impaired immune functions in zinc deficiency syndromes are described. The regulation of innate immunity as well as the function and maturation of lymphocytes and monocytes is critically discussed as a system dependent on the zinc concentration in vivo and in vitro. Furthermore, the influence of zinc on experimental systems as well as on widely used immunostimulants is described, showing the importance of the knowledge of zinc concentration in in vitro leukocyte studies. The specific interactions of zinc with immunologically important serum proteins, signal transduction components, and membrane functions is summarized, showing the molecular basis of this interaction as known so far. Finally, the therapeutic use of zinc is critically discussed with new aspects also using the immunosuppressive effects of zinc. In conclusion, these data show that the zinc concentration should be taken into account whenever complex alterations of immune functions are observed. J. Leukoc. Biol. 64: 571–577; 1998.
Instillation of allogeneic lung macrophages and dendritic cells cause differential effects on local IFN-7 production, lymphocytic bronchitis, and vasculitis in recipient murine lungs
Authors: Wilkes David S , Thompson Linda K , Cummings Oscar W , Bragg Shanda , Heidler Kathleen M 
Published: January 2018

Abstract
Lung allograft rejection is believed to be initiated by donor lung accessory cells, namely macrophages and dendritic cells, interacting with recipient lymphocytes leading to up-regulated Th1 type (IFN-γ) cellular immunity culminating in graft destruction. The purpose of this study was to determine the individual role of donor lung macrophages and dendritic cells in the rejection response. Utilizing a murine model that reproduces the immunology and histology of acute rejection, C57BL/6 mouse (I-ab, H-2b) lung dendritic cells (DC-enriched lung cells), purified alveolar macrophages (I-a-negative macrophages), or various ratios of I-a-negative macrophages/DC were instilled into BALB/c mouse (I-ad, H-2d) lungs followed by an assessment of local IFN-γ production and grading of rejection pathology. The data show that DC, and not I-a-negative macrophages, induced IFN-γ production in recipient lungs. However, the local production of IFN-γ was not always associated with histological changes characteristic of rejection pathology. In contrast to either cell type alone, instillation of C57BL/6 I-a-negative macrophages and DC, together, were required to induce rejection pathology in BALB/c lungs. In addition, the rejection response was dependent on interactions between donor I-a-negative macrophages and DC. J. Leukoc. Biol. 64: 578–586; 1998.
The murine homolog of the HIN 200 family, Ifi 204, is constitutively expressed in myeloid cells and selectively induced in the monocyte/macrophage lineage
Authors: Gariglio Marisa , De Andrea, Marco , Lembo Marianna , Ravotto Monica , Zappador Claudio , Valente Guido , Landolfo Santo 
Published: January 2018

Abstract
To examine the expression of Ifi 200 genes in vivo and add new information about their function, polyclonal monospecific rabbit antibodies, designated N-term or C-term, were raised against both the N-terminus and C-terminus of the 204 protein (p204) respectively. Western blotting analysis demonstrated that p204 and D3, another member of the Ifi 200 gene family, are constitutively expressed, though at different degrees, in bone marrow, thymus and lymph nodes, and barely detectable in the spleen. Poly rI:rC treatment did not modulate their expression. Peritoneal resident macrophages (Mϕ) from untreated mice were negative, but displayed high levels of both p204 and D3 on poly rI:rC treatment. A significant increase of these proteins is also observed when Mϕ are cultured overnight in vitro with IFNs or LPS. Lung, kidney and brain were negative for p204 and D3 expression. These results, together with immunois-tochemical analysis, demonstrate that the 204 gene has an expression pattern restricted to cells of the myelomonocytic lineage similar to that observed for the human homolog, the myeloid nuclear differentiation antigen (MNDA) suggesting its potential involvement in the differentiation and maturation of this cell lineage. J. Leukoc. Biol. 64: 608–614; 1998.
Effects of platelet release products on neutrophilic Fcγ receptors
Authors: Sakamoto Noriko , Sakamoto Haruhiko , Tanaka Sumiko , Oryu Makoto , Ogawa Yoshitada 
Published: January 2018

Abstract
Large and small macromolecular activators of phagocytosis from platelets (l-MAPP and s-MAPP, respectively), which function via the neutrophilic Fcy receptors (FcγR) were refined from platelet release products by gel filtration and affinity chromatography with the use of an anti transferrin antibody column and the mechanism of phagocytosis activation was investigated. Flow cytometry revealed that l-MAPP and s-MAPP did not increase the expression of neutrophilic FcγRII (CD32) and FcγRIII (CD16) antigens, whereas rosette formation of neutrophils with rabbit IgG-sensitized sheep erythrocytes (EA) in the presence of anti FcγR antibodies suggested that both MAPPs increase the binding ability of FcγRII. On the other hand, the enhancing effect of l-MAPP and s-MAPP on neutrophilic phagocytosis disappeared with the increase in phagocytosis by the phosphate-buffered saline control neutrophils when they were centrifuged with EA before incubation for phagocytosis. The enhanced phagocytosis, both by the two MAPPs and centrifugation, was canceled by treatment of the neutrophils with anti-CD32 Fab. The phagocytosis activatory effects of MAPP on neutrophils were canceled by anti-CD71 monoclonal antibody but not by transferrin. J. Leukoc. Biol. 64: 631–635; 1998.
Signaling in neuropeptide-induced migration of human eosinophils
Authors: Dunzendorfer Stefan , Meierhofer Christian , Wiedermann Christian J 
Published: January 2018

Abstract
At inflammatory sites, leukocytes may confront multiple, competing chemoattractive signals. We compared the chemotactic potencies of several sensory neuropeptides with regard to signal transduction pathways in eosinophils. Eosinophils were enriched using magnetic cell sorting and migration was assayed in a Boyden microchemotaxis chamber. We found stimulatory effects of substance P, calcitonin gene-related peptide (CGRP), secretoneurin, vasoactive intestinal peptide (VIP), and secretin on eosinophil migration. Actions of VIP are predominantly mediated via VIP receptor type I. Migration toward secretoneurin, VIP, and secretin was blocked by a phosphodiesterase inhibitor, which, in contrast failed to affect substance P- and CGRP-induced eosinophil chemotaxis. Wortmannin blunted the migratory responses induced by all neuropeptides tested and substance P-induced effects on eosinophils were tyrphostin-23-sensitive. We conclude that substance P, CGRP, secretoneurin, and VIP/secretin stimulate eosinophil migration involving wortmannin-sensitive enzymes. Moreover, secretoneurin and VIP/secretin require additional activation of phosphodiesterases to stimulate eosinophil migration. J. Leukoc. Biol. 64:828–834; 1998.
Bacterial phagocytosis activates extracellular signal-regulated kinase and p38 mitogen-activated protein kinase cascades in human neutrophils
Authors: McLeish Kenneth R , Klein Jon B , Coxon Patricia Y , Head Kimberly Z , Ward Richard A 
Published: January 2018

Abstract
The hypothesis that bacterial phagocytosis by human polymorphonuclear neutrophils (PMNs) stimulates MAPK cascades that regulate respiratory burst activation was tested. Extracellular response kinase (ERK) and p38 kinase, but not c-Jun NH2-terminal kinase, activities were increased within 5 min of phagocytosis of plasma-opsonized Staphylococcus aureus (S-SA), reached maximum at 20–30 min, and remained elevated through 60 min. The role of Fcγ receptors was examined using gamma globulin-opsonized SA (IgG-SA), whereas CR3 receptors were activated by particulate β-glucan. IgG-SA stimulated a maximal ERK activity at 30 min, whereas p38 activity was maximal at 5 min. β-glucan stimulated maximal ERK activity at 5 min and maximal p38 activity at 2 min. Non-opsonized bacteria were ingested at 10% of the level of S-SA and stimulated a minimal increase in ERK and p38 activity at 60 min. S-SA stimulation of ERK was inhibited by wortmannin, LY294002, and genistein, but not calphostin C; whereas p38 stimulation was inhibited by calphostin C and genistein, but not wortmannin and LY294002. Simultaneous measurement of phagocytosis and H2O2 production by flow cytometry was used to assess the role of ERKs and p38 kinase in phagocytosis. The MEK inhibitor PD098059 had no significant effect on phagocytosis or H2O2 production. The p38 kinase inhibitor SB203580 significantly attenuated H2O2 production, whereas phagocytosis was unaffected. In conclusion, bacterial phagocytosis stimulates ERK and p38 activation by distinct signal transduction pathways. Phagocytosis-stimulated p38 kinase activity is necessary for optimal H2O2 production. J. Leukoc. Biol. 64: 835–844; 1998.
MIC-1 is a novel TGF-β superfamily cytokine associated with macrophage activation
Authors: Fairlie W D , Moore A G , Bauskin A R , Russell P K , Zhang H-P , Breit S N 
Published: January 2018

Abstract
As part of a study to identify novel genes associated with macrophage activation, we have cloned a new member of the transforming growth factor β (TGF-β) superfamily designated macrophage inhibitory cytokine 1 (MIC-1). MIC-1 is synthesized as a 62-kDa intracellular protein, which, after cleavage by a furin like protease, is secreted as a 25-kDa disulfide-linked dimeric protein. Sequence analysis indicates that it does not cluster within any existing TGF-β families, suggesting it may be the first member of a new grouping within the TGF-β superfamily. Tissue Northern blots show that MIC-1 transcripts are only found abundantly in placenta, although smaller amounts are seen in a limited number of other adult and fetal tissues. MIC-1 is not expressed in resting macrophages but is induced by a number of different activation agents, including phorbol myristate acetate, interleukin 1, tumor necrosis factor α, and macrophage colony-stimulating factor but not by lipopolysaccharide or interferon-γ. We have hypothesized that it may be an autocrine inhibitor of macrophage activation but its major biological role is still uncertain. J. Leukoc. Biol. 65: 2–5; 1999.
The cell biology of leukocyte-mediated proteolysis
Authors: Owen Caroline A , Campbell Edward J 
Published: January 2018

Abstract
Leukocyte-derived proteinases have the capacity to degrade every component of the extracellular matrix, and thereby play fundamental roles in physiological processes. However, if the activity of these proteinases is uncontrolled or dysregulated, they have the capacity to contribute to tissue injury that potentially affects every organ in the body. Although there is a substantial literature on structure and activity of these proteinases when they are free in solution, until recently there has been little information about the cell biology of proteinases and their inhibitors. Recent studies, however, have identified several mechanisms by which inflammatory cells can degrade extracellular proteins in a milieu that contains high-affinity proteinase inhibitors. J. Leukoc. Biol. 65: 137–150; 1999.
Selective antibody blockade of lymphocyte migration to mucosal sites and mast cell adhesion
Authors: Palecanda Aiyappa , Marshall Jean S , Li Xian , Briskin Michael J , Issekutz Thomas B 
Published: January 2018

Abstract
The integrins α4β7 and α4β1 mediate adhesion to the mucosal addressin cell adhesion molecule-1 (MAdCAM-1) and the vascular cell adhesion molecule-1 (VCAM-1) and are important in T cell and allergic inflammatory reactions in the rat. The relative contributions of α4β7 and α4β1 in these reactions is unknown. To examine the role of α4β7 in the rat a new mAb, TA-6, was developed. TA-6 inhibited adhesion to MAdCAM-1 but not to VCAM-1, a characteristic of α4β7 adhesion, and immunofluorescence and immunoprecipitation studies were compatible with binding to α4β7. TA-6 blocked rat lymphocyte adhesion to mesenteric lymph nodes and T cell migration to mucosal lymphoid tissues and it bound to rat mucosal mast cells. TA-6 did not inhibit lymphocyte adhesion to peripheral lymph nodes and T cell migration to peripheral lymphoid tissues or cutaneous inflammatory sites, and was not expressed on connective tissue mast cells. J. Leukoc. Biol. 65: 649–657; 1999.
MCP-1 is selectively expressed in the late phase by cytokine-stimulated human neutrophils: TNF-α plays a role in maximal MCP-1 mRNA expression
Authors: Yamashiro Shigeo , Kamohara Hidenobu , Yoshimura Teizo 
Published: January 2018

Abstract
Culture supernatants of phytohemagglutinin (PHA)-stimulated human peripheral blood mononuclear cells (PHA-sup) induced monocyte chemoattractant protein-1 (MCP-1) mRNA expression in human neutrophils. MCP-1 mRNA was first detected by Northern analysis at 8 h, and the peak level was detected at 16 h and sustained until 72 h. Cycloheximide and genistein, but not pertussis toxin, inhibited the expression of MCP-1 mRNA. Recombinant tumor necrosis factor α (TNF-α) induced a low level MCP-1 mRNA accumulation in neutrophils, and addition of anti-TNF-α IgG blocked 30–70% of MCP-1 mRNA expression induced with PHA-sup. PHA-sup-stimulated PMN synthesized and secreted 3.1 ± 1.3 ng/5 × 106 PMN MCP-1 within the first 24 h. Hybridization of 32P-labeled cDNA preparations to an array of human cytokine cDNAs further indicated that MCP-1 mRNA was selectively up-regulated in the late phase after stimulation with the PHA-sup. J. Leukoc. Biol. 65: 671–679; 1999.