bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expression of cytokine mRNA in murine splenic dendritic cells and better induction of T cell-derived cytokines by dendritic cells than by macrophages during in vitro costimulation assay using specific antigens
Authors: Kanangat Sivadasan , Nair Smita , Babu John Sam , Rouse Barry T 
Published: January 2018

Abstract
Among antigen-presenting cells dendritic cells (DC) have the unique ability to generate primary T cell response. The reasons for the superior inductive property of DC still remain obscure. The explanations offered include higher expression of CD80, MHCII, and ICAMI on DC surface which allows effective cluster formation with T cells. It is also possible that additional cellular characteristics of DC, i.e., their ability to release critical mediators involved in the induction of effective immune response, are important. We examined the ability of DC to express IL-1, IL-6, and IL-12 using the highly sensitive reverse transcription-quantitative polymerase chain reaction. Our data show that highly purified (97–99% pure) murine splenic DC were capable of expressing IL-1, IL-6 and IL-12 mRNA upon stimulation with lipopolysaccharide. We also compared the ability of DC and macrophages to induce T cell-derived cytokines IL-2 and IFN-γ in an in vitro antigen-specific costimulation assay. In naive T cells stimulated with antigen presented via DC or macrophages, the levels of mRNA for IL-2 and IFN-γ were 2- to 4-fold higher when cells were stimulated with DC. Overall, our data add additional support to the description of DC as superior antigen-presenting cells for the activation of naive T cells. J. Leukoc. Biol. 57: 310–316; 1995.
Neutrophil activation by anti-β2 glycoprotein I monoclonal antibodies via Fcγ receptor II
Authors: Arvieux Josiane , Jacob Marie-Christine , Roussel Bernard , Bensa Jean-Claude , Colomb Maurice G 
Published: January 2018

Abstract
Murine monoclonal antibodies (mAbs) to human β 2-glycoprotein I (β 2GPI), a plasma protein required for the binding of some antiphospholipid antibodies, have been shown to possess lupus anticoagulant properties and to activate platelets via Fcγ receptor (FcγR) crosslinking. Here we investigated their ability to induce polymorphonuclear leukocyte (PMN) functional responses. The six mAbs (IgGl isotype) tested in combination with β 2GPI led to a concentration-dependent activation of human PMNs as appreciated by granule release, H2O2 production, and cytosolic Ca2+ increase. This activation process was accompanied by the enhancement of PMN-mediated heparan sulfate loss from the endothelial cell line EA.hy 926 without evidence for cell lysis or detachment. F(ab’)2 fragments of one of the mAbs bound to PMNs in a β 2GPI-dependent manner but were devoid of activating effects. Carbamylated β 2GPI was unable to mediate PMN-antibody binding and subsequent activation. In addition, cationization of β 2GPI or removal of its sialic acid groups led to higher efficiency in binding to the PMN surface and triggering activation in comparison with the untreated protein. Thus, the process of PMN activation depends on mAb binding to these cells through both Fab (via β 2GPI) and Fc domains, as confirmed by the suppression of all responses upon treatment with an anti-FcγRII, but not anti-FcγRIII, antibody. Our data suggest a model of cellular activation by β 2GPI-dependent antiphospholipid antibodies. J. Leukoc. Biol. 57: 387–394; 1995.
Retinoic acid inhibits basal and interferon-γ-induced expression of intercellular adhesion molecule 1 in monocytic cells
Authors: Weber Christian , Calzada-Wack Julia C , Goretzki Michael , Pietsch Angelika , Johnson Judith P , Ziegler-Heitbrock H W Löms 
Published: January 2018

Abstract
Retinoic acid (RA) and 1,25-(OH)2-vitamin D3 (1,25-D3) induced U937 cell maturation into distinct monocytic phenotypes, as demonstrated by up-regulation of CD23 by RA and CD14 by 1,25-D3. Differentiation by RA but not by 1,25-D3 was associated with reduction of basal and complete suppression of interferon-γ (IFN-γ)–stimulated intercellular adhesion molecule 1 (ICAM-1) expression. Induction of cyclooxygenase activity by RA and attenuation of basal ICAM-1 expression exhibited similar kinetics. Treatment with indomethacin prevented and prostaglandin E2 (PGE2), dibutyryl-cAMP, or forskolin mimicked reduction of basal ICAM-1 expression by RA, indicating that this effect of RA is mediated by PGE2 synthesis and subsequent cAMP elevation. In contrast, suppression of IFN-γ-induced ICAM-1 expression by RA was only partly reversible by indomethacin, suggesting that inhibition of IFN-γ stimulation was not completely due to cyclooxygenase induction. RA did not always counteract IFN-γ, as it cooperated with IFN-γ in down-regulating very late activation antigen 4. Specific polymerase chain reaction and Northern blotting of ICAM-1 mRNA revealed that RA suppressed ICAM-1 induction by IFN-γ at the transcriptional level. RA also blocked ICAM-1 induction by IFN-γ in isolated human blood monocytes. In conclusion, inhibition of basal and stimulated ICAM-1 expression in monocytic cells may provide a mechanism for beneficial anti-inflammatory effects of retinoids. J. Leukoc. Biol. 57: 401–406; 1995.
T cells and HIV-induced T cell syncytia exhibit the same motility cycle
Authors: Sylwester Andrew , Shutt Damon , Wessels Deborah , Stapleton Jack T , Stites Jan , Kennedy Ronald C , Soil David R 
Published: January 2018

Abstract
Ameboid cells ranging in complexity from Dictyostelsum amebas to human polymorphonuclear leu kocytes (PMNs) translocate in a cyclical fashion. Using computer-assisted motion analysis, we have analyzed the motility of human lymphocytes of the immortal SupTl cell line and of a peripheral blood mononuclear cell popu lation highly enriched for CD4-positive cells (CD4-enriched PBMCs) on four substrates—plastic, dehydrated rat tail collagen, hydrated rat tail collagen, and bovine aortic en dothelium. In addition, we have analyzed the motility on these substrates of syncytia induced by human immuno deficiency virus (HIV) in cultures of both cell types. It is demonstrated that both SupTl cells and CD4-enriched PBMCs exhibit a motility cycle with a period of 1.6 min that is independent of substrate, independent of average cell velocity, and similar to the periods of translocating Dictyostelium amebas and PMNs. More surprisingly, it is demonstrated that HIV-induced SupTl and PBMG syn cytia with volumes 10 to 100 times those of single cells ex hibit the same motility cycle as their single-cell progeni tors. These observations support the generality of the motility cycle in animal cells and, for the first time, demonstrate that the cycic is independent of cell size. J. Lcukoc. BioL 57; 643–650; 1995.
CD30 and type 2 T helper (Th2) responses
Authors: Romagnani Sergio , Del Prete Gianfranco , Maggi Enrico , Chilosi Marco , Caligaris-Cappio Federico , Pizzolo Giovanni 
Published: January 2018

Abstract
CD30 is one of the members of the tumor necrosis factor receptor superfamily, originally described as a marker of Reed-Sternberg and Hodgkin’s cells in Hodgkin’s lymphoma. CD30 appears to be preferentially expressed on, and its soluble form (sCD30) released by, CD4+ and CD8+ T cell clones capable of producing T helper 2 (Th2)-type cytokines. In nonneoplastic conditions, CD30+ T cells are barely detectable in vivo; however, a few allergen-specific CD4+CD30+ T cells inducible to the production of Th2-type cytokines could be sorted out from the circulation of allergic subjects after allergen exposure. Moreover, high numbers of CD30+ T cells were found in the lymph node of a patient suffering from Omenn’s syndrome, a rare congenital Th2-mediated immunodeficiency disorder. More importantly, high serum levels of sCD30 were observed in some conditions in which a pathogenetic role for Th2 cells has been suggested, such as Omenn’s syndrome, atopy, systemic lupus erythematosus, and after infection with measles virus or human immunodeficiency virus. Thus, detection of CD30+ T cells and/or of increased levels of sCD30 may reflect the presence of immune responses or immune alterations characterized by the prevalent activation of Th2-like cells. J. Leukoc. Biol. 57: 726-730; 1995.
Matrix metalloproteinases and processing of pro-TNF-α
Authors: Gearing A J H , Beckett P , Christodoulou M , Churchill M , Clements J M , Crimmin M , Davidson A H , Drummond A H , Gallowav W A , Gilbert R , Gordon J L , Leber T M , Mangan M , Miller K , Nayee P , Owen K , Patel S , Thomas W , Wells G , Wood L M , Woolley K 
Published: January 2018

Abstract
Tumor necrosis factor-α (TNF-α) is released from a cell membrane-anchored precursor by proteolytic cleavage. We have shown that broad spectrum synthetic inhibitors of matrix metalloproteinases (MMPs) prevent the processing of the TNF precursor but do not inhibit the release of other cytokines. Purified MMPs, stromelysin, matrilysin, collagenase, and the gelatinases can all cleave a recombinant pro-TNF substrate to yield mature TNF. MMP inhibitors prevent the rise in blood levels of TNF after endotoxin administration in rats and are effective in animal models of inflammatory disease such as adjuvant arthritis. Drugs that inhibit MMP action and TNF release show great promise for the treatment of autoimmune inflammatory diseases. J. Leukoc. Biol. 57: 774–777; 1995.
Bicarbonate and phosphate ions protect transferrin from myeloperoxidase-mediated damage
Authors: Edeker Brian L , Rasmussen George T , Britigan Bradley E 
Published: January 2018

Abstract
Exposure to hypochlorous acid (HOC1), the main product of the reaction of neutrophil myeloperoxidase (MPO), H2O2, and Cl-, reportedly decreases apotransferrin’s iron binding capacity. Optimal transferrin iron binding requires the coexistent binding of anions such as bicarbonate (HCO3-) near the protein’s two iron binding sites. Recently, we found that if HCO3- was also present during HOC1 exposure, apotransferrin retained its ability to inhibit iron-catalyzed hydroxyl radical generation. Therefore, we examined apotransferrin iron binding capacity after exposure to the MPO/H2O2/I- system in the presence and absence of several anions (HCO3-, H2PO4-, SO42-, and ClO4-) known to bind to apotransferrin. Although the MPO system decreased apotransferrin iron uptake to only 46% of the untreated apotransferrin control, apotransferrin treated in the presence of 1 mM HCO3- or H2PO4- retained 84 and 74%, respectively, of its iron binding capacity. Similar results were seen when apotransferrin was treated with NaOCl. These results could not be explained on the basis of a loss of MPO activity or scavenging of HOCl. In contrast, SO42- and ClO4- were unable to prevent the MPO-mediated loss of apotransferrin iron binding capacity. NaOCl had no effect on the ability of transferrin to bind any of these anions, as assessed by the anion-induced change in apotransferrin absorbance spectrum. HCO3- but not H2PO4-, SO42-, or ClO4- decreased MPO-mediated oxidation (iodination) of apotransferrin. Under some conditions H2PO4- actually increased apotransferrin iodination. HCO3- and H2PO4- may protect apotransferrin from MPO-mediated oxidative damage by preventing selective oxidation of one or both iron binding sites. This process may allow transferrin to retain its iron binding function during MPO exposure in vivo. J. Leukoc. Biol. 58: 59–64; 1995.
CD4+ contrasuppressor T cells improve the resistance of thermally injured mice infected with HSV
Authors: Kobayashi Makiko , Hemdon David N , Pollard Richard B , Suzuki Fujio 
Published: January 2018

Abstract
Modulation of burn-associated CD8+ CD11b+ T cell receptorγ/δ+ suppressor T cells (BA2T cells) and improved resistance to herpesvirus infections was studied in thermally injured mice. The susceptibility of thermally injured mice to infection by herpes simplex virus (HSV) was approximately 100 times greater than it was in normal mice. The increased susceptibility of thermally injured mice to HSV infection was transferred to normal mice by BA2T cells, which appeared in spleens of mice 2–9 days after thermal injury. The suppressor cell activity of BA2T cells was effectively counteracted by CD4+ CD28+ T cell receptorα/β+ Vicia villosa lectin adherent antisuppressor cells (designated as bum-induced contrasuppressor T cells; BCS cells), which were generated naturally in spleens of mice after the appearance of BA2T cells. The adoptive transfer of BCS cells to mice just after the injury improved the resistance of thermally injured mice to HSV infection to levels observed in normal mice. These results suggest that the increased susceptibility of thermally injured mice to HSV infection may be affected by BA2T suppressor cells and BCS cells may improve the resistance of thermally injured mice to HSV infection through the inhibition of BA2T suppressor cell activities. J. Leukoc. Biol. 58: 159–167; 1995.
Migration of distinct subsets of CD8+ blood T cells through endothelial cell monolayers in vitro
Authors: Berman Jeffrey S , Mahoney Kathleen , Saukkonen Jussi J , Masuyama Junichi 
Published: January 2018

Abstract
The immune response in many infections and to allografts is dependent on CD8+ cytotoxic T lymphocytes (CTL). Influx of CD8+ CTL from the blood has been documented during antigen challenge. We have previously found that a subset of CD8+ T cells from normal blood can migrate through endothelial cell monolayers in vitro. To further characterize migration-prone CD8+ T cells from normal blood, we examined the expression of CD28 and a restricted epitope of CD18/CD11a (S6F1), a CTL marker. Although normal blood CD8bright+ T cells were heterogeneous in their expression of CD28, three populations could be identified (CD28low, CD28moderate, and CD28high). CD8+ cells migrating across endothelial cell monolayers were enriched for CD8bright+ CD28high cells and a subset of CD8dim+ cells, which were CD28high. Both adherent and migrating CD8+ cells were exclusively (&gt;95%) S6F1high. There was also preferential adhesion and migration of CD8+ cells expressing the low-molecular-weight form of the leukocyte common antigen, CD45RO. Cytokine activation of the endothelium did not significantly alter preferential migration of these subsets. These data suggest that certain subsets of CD8+ memory T cells in normal human blood are prone to, adhere to, and migrate through allogeneic endothelial cells and would thus be likely to be recruited to sites of antigen challenge.
Desensitization of the actin polymerization response in human neutrophils at low cell density
Authors: Model Michael A , Omann Geneva M 
Published: January 2018

Abstract
Many chemoattractant-activated responses in neutrophils show transient kinetics, suggesting that rapid desensitization occurs during the time course of the response. We found that desensitization of the actin polymerization response to N-formyl peptides is, in a large part, due to inhibition by adenosine released from cells to the medium and depletion or a chemical inactivation of the agonist. To reduce the influence of these factors, we stimulated neutrophils in a very diluted suspension, sometimes with continuous replacement of the medium. The actin polymerization response to a high agonist concentration was greatly enhanced and prolonged under these conditions, often without any tendency to subside within 10 min at 25°C. It has previously been shown that the N-formyl peptide receptor converts from a rapidly dissociating to a slowly dissociating and presumably inactive form during activation. Under the conditions of low cell concentration, the conversion to a slowly dissociating receptor still occurred. Thus the prolonged response was not due to prolonged presence of rapidly dissociating receptors. We conclude either that a low number of rapidly dissociating receptors, which we failed to see, is sufficient to maintain actin polymerization or that slowly dissociating receptors can support the actin response. In contrast to responses stimulated by high agonist concentrations, the responses to low concentrations of the agonists were transient. The results of other authors indicate that low concentrations of N-formyl peptides do not desensitize the receptors. Other mechanisms, which are specific for the actin polymerization response, must be involved in response termination to low concentrations of N-formyl peptides. Activation at low cell density will be a useful approach for studying other processes (Ca2+ elevation, oxidant production, etc.) and chemoattractants (leukotriene B4, interleukin 8, etc.) for which an understanding of the kinetics due to desensitization of the components of the receptor-mediated activation pathway is desired.
Inhibition of superantigen-induced T cell proliferation and monocyte IL-1β, TNF-α, and IL-6 production by acute ethanol treatment
Authors: Szabo Gyongyi , Mandrekar Pranoti , Catalano Donna 
Published: January 2018

Abstract
Alcohol use has been shown to decrease monocyte antigen presentation capacity and inflammatory cytokine production, thereby increasing susceptibility to infections. Here, we demonstrate that in vitro acute treatment of normal monocytes with pharmacological doses of ethanol can decrease superantigen [Staphylococcus enterotoxins B (SEB) and A (SEA)]-induced T cell proliferation. Furthermore, ethanol treatment (25–100 mM) significantly inhibited SEA- or SEB-induced production of tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), and IL-6 in monocytes. Ethanol-induced down-regulation of monocyte TNF-α, IL-1β, and IL-6 occurred at both the protein and mRNA levels. Additional data suggest that ethanol can decrease IL-1β mRNA stability. Furthermore, experiments using cycloheximide indicate that de novo protein synthesis is required for the inhibitory effect of ethanol on SEB-induced IL-1β mRNA production. Finally, ethanol treatment decreased HLA-DR expression in monocytes, suggesting that ethanol treatment can compromise monocyte stimulation by down-regulating the SEB-binding capacity of monocytes. These results suggest that acute ethanol treatment can interfere with monocyte activation by SEB at multiple steps. Consequently, decreased superantigen-induced polyclonal T cell activation and inflammatory monokine production would contribute to an impaired immune response to bacterial challenge with superantigens after acute alcohol intake.
Monomeric human IgE evokes a transient calcium rise in individual human neutrophils
Authors: Collison Kate S , Kvvaasi Aaron A A , Parhar Ranjit S , Al-Sedairy Sultan T , Al-Mohanna Futwan A A 
Published: January 2018

Abstract
Digital fluorescence calcium imaging was used to investigate and identify the primary biological responses of human neutrophils to monomeric immunoglobulin E (IgE). Treatment of neutrophils with IgE caused a transient rise in the level of intracellular calcium that was inhibited by pertussis toxin. The calcium rise was due mainly to release from an intracellular membrane-enclosed store that is also sensitive to the chemotactic peptide formyl-Met-Leu-Phe. The IgE-induced calcium transient was independent of Fcγ receptors and of Fc receptor ligation. Our data suggest that the mere binding of IgE to neutrophils is sufficient to evoke a biological response without the need for IgE/receptor cross-linking.
Regulation of N-formyl-methionyl-leucyl-phenylalanine receptor recycling by surface membrane neutral endopeptidase–-mediated degradation of ligand
Authors: Painter Richard G , Aiken Martha L 
Published: January 2018

Abstract
Neutrophil responses to α-N-formyl-L-Met- L-Leu-L-Phe (fMLF) are modulated by inhibitors of surface membrane neutral endopeptidase (NEP), such as phosphoramidon (PPAD). Because receptor recycling is presumably required for a sustained cellular response, the effect of PPAD on receptor reexpression was examined. After down-regulation of surface fMLF receptors by fMLF, PPAD blocked the normal reexpression of surface receptors in a manner that was related to the time of prior exposure to fMLF. Internalized fML[3H]F was hydrolyzed by NEP at a rate comparable to the rate of receptor reexpression at the cell surface, suggesting that ligand hydrolysis is rate limiting. To test this hypothesis, cells were incubated with fluorescein-labeled formyl-Met-Leu-Phe-Nle-Tyr-Lys at 15°C. After binding was complete, but before internalization of receptor-ligand complexes, high-affinity antifluorescein antibody F(ab’)2 fragments were added and the cells incubated at 37°C for 60 min in the presence of PPAD. Under these conditions, the inhibitory effects of PPAD were largely reversed and nonimmune F(ab’)2 fragments were without effect.
A role for a 70-kDa amino-terminal fibronectin fragment in supporting soluble gelatin interactions with rat peritoneal macrophages
Authors: Penc S F , Blumenstock F A , Kaplan J E 
Published: January 2018

Abstract
Seventy-kilodalton amino-terminal and 180-kDa cell-binding fibronectin fragments were used to determine which fibronectin domains support soluble gelatin interactions with macrophages. At each time measured, intact and 180-kDa fibronectin supported significantly larger quantities of cell-associated gelatin than control levels (P &lt; 0.05). Throughout the time course fibronectin supported more binding than 180 kDa. Seventy kilodalton did not augment gelatin binding until 2 h, but by 6 h 70 kDa supported more binding than intact fibronectin (P &lt; 0.01). This appeared to result from a cellular response initiated by 70-kDa-gelatin interactions with the macrophages. Within 4 h the majority of gelatin associated with cells under control conditions, and in the presence of fibronectin or 180 kDa, was internalized. Seventy-kilodalton-mediated binding remained localized primarily to the cell surfaces at all times. The macrophages partially degraded the internalized and external gelatin fractions. These results demonstrate that intact fibronectin and specific fibronectin fragments support soluble gelatin interactions with macrophages.
The amyloidogenic peptide human amylin augments the inflammatory activities of eosinophils
Authors: Horn Joanne T , Estridge Tom , Pechous Penni , Hyslop Paul A 
Published: January 2018

Abstract
The amyloidogenic peptides, amyloid-β (Aβ) and human amylin, are the major constituents of amyloid deposits found in patients with the chronic degenerative disorders Alzheimer’s disease (AD) and type 2 diabetes, respectively. Recent studies have shown that a variety of inflammatory proteins such as cytokines are associated with the amyloid deposits of AD brain tissues. Therefore, in the present study, we sought to determine whether Aβ and/or human amylin could modulate the various inflammatory activities of eosinophils. We observed that human amylin but not Aβ peptides inhibited the in vitro interleukin-5 (IL-5)–mediated survival of cord blood–derived eosinophils (CBEs) in a concentration-dependent manner. By contrast, rat amylin, a nonamyloidogenic peptide that is highly homologous to human amylin, failed to affect the IL-5–mediated survival of CBEs. Similar inhibitory effects of human amylin were observed for peripheral blood eosinophils. Human amylin also enhanced the release of the cytokine granulocyte-macrophage colony-stimulating factor by CBEs that were stimulated with the calcium ionophore A23187 but was incapable of directly stimulating CBEs to release cytokines. In addition, the A23187-induced release of the inflammatory lipid mediator leukotriene C4 by CBEs was augmented by human amylin. These results suggest that the amyloidogenic peptide human amylin is capable of amplifying the various inflammatory activities of eosinophils.