bluuebunny/crossref_metadata_2025_split huggingface dataset:
Role of cytokines in epidermal Langerhans cell migration
Authors: Wang Binghe , Amerio Paolo , Sauder Daniel N 
Published: January 2018

Abstract
In the epidermal compartment of skin, keratinocytes (KC), Langerhans cells (LC), and their soluble products, i.e. cytokines, constitute a unique immunologic microenvironment. KC participate in cutaneous immune responses by producing various cytokines. LC, a member of the dendritic cell (DC) family, represent the professional antigen-presenting cells in the epidermis. Although it has been demonstrated that migration of LC from skin to lymph nodes is a critical step for the antigen presentation, molecular mechanisms for such an event remain unclear. Recent studies suggest that cytokines are able to modulate LC/DC migration. There is accumulating evidence that proinflammatory cytokines including interleukin (IL)-1 and tumor necrosis factor a promote LC emigration from the skin, whereas the anti-inflammatory cytokine IL-10 is a counter-regulator. LC/DC express chemokine receptors. Chemokines generated from lymphatic endothelial cells and lymph node cells play a role in the directional migration of LC/DC into lymph nodes. This article reviews current studies on the role of cytokines in LC/DC migration. J. Leukoc. Biol. 66: 33–39; 1999.
Interleukin-18 synthesis and secretion by dendritic cells are modulated by interaction with antigen-specific T cells
Authors: Gardella Stefania , Andrei Cristina , Costigliolo Sara , Poggi Alessandro , Zocchi M Raffaella , Rubartelli Anna 
Published: January 2018

Abstract
We show that interleukin-18 is constitutively produced by dendritic cells; synthesis and secretion are poorly affected by maturative stimuli. Challenge of dendritic cells with autologous antitetanus toxoid T lymphocytes results in a secretory switch, with induction of secretion of biologically active interleukin-18 and decrease of its intracellular content. Similarly, when dendritic cells are challenged with allospecific T cells a dramatic decrease of intracellular interleukin-18 content occurs, whereas no effects are observed after co-culture with autologous activated T cells. The induction of secretion can be mediated by engagement of CD40 on dendritic cells, as indicated by the increased amount of interleukin-18 in dendritic cell supernatants after CD40 triggering by anti-CD40 antibodies. However, CD40 engagement, unlike from antigen-specific T cells, does not result in reduced intracellular interleukin-18 content, suggesting that this decrease may be mediated by structure(s) involved in antigen recognition. J. Leukoc. Biol. 66: 237–241; 1999.
Role of antigen-presenting cells in cross-priming of cytotoxic T lymphocytes by apoptotic cells
Authors: Ronchetti Anna , Iezzi Giandomenica , Crosti Maria Cristina , Garancini Maria Paola , Protti Maria Pia , Bellone Matteo 
Published: January 2018

Abstract
Although the mechanisms regulating recognition and phagocytosis of apoptotic cells by scavenger cells are the subject of intense investigation, little is known about the fate of the antigens contained in apoptotic cells and the constraints defining their immunogenicity. We developed a model in C57BL/6 mice to evaluate whether phagocytosis of apoptotic tumor cells yielded antigens able to get access to the MHC class I pathway and activate a specific cytotoxic T lymphocyte response. Our results demonstrate that apoptotic tumor cells are antigenic in vitro and can be immunogenic in vivo. Their immunogenicity depends on the number of cells used for immunization and the antigen-presenting cells involved in processing and presentation of antigens contained in the dying cells. The demonstration of the immunogenicity of apoptotic cells may have direct implications both in autoimmunity and cancer. J. Leukoc. Biol. 66: 247–251; 1999.
The role of dendritic cells in T cell selection and survival
Authors: Brocker Thomas 
Published: January 2018

Abstract
Dendritic cells (DC) not only play an important role in the induction of immunity, but also have major functions in thymus and periphery in the absence of nominal antigen. In order to study these and other DC-functions in vivo, we expressed MHC class II I-E molecules under the control of the DC-specific CD11c promoter in C57Bl/6 mice. With this targeted expression we were able to investigate DC functions in vivo without further manipulation of DC. We describe our findings with respect to the two major thymic events of negative and positive selection and demonstrate that DC are able and sufficient to induce negative selection of autoreactive CD4+ thymocytes by clonal deletion but do not induce positive selection. We further demonstrate in thymus-transplant experiments that DC play a major role in inducing survival of peripheral CD4+ mature T cells. This transgenic model therefore seems to be a valuable tool for the investigation of DC functions in vivo. J. Leukoc. Biol. 66: 331–335; 1999.
IL-6 knock-out mice exhibit resistance to splanchnic artery occlusion shock
Authors: Cuzzocrea Salvatore , De Sarro Giovambattista , Costantino Giuseppina , Ciliberto Gennaro , Mazzon Emanuela , De Sarro Angela , Caputi Achille P 
Published: January 2018

Abstract
We used IL-6 knock-out (KO) mice to evaluate a possible role for IL-6 in the pathogenesis of splanchnic artery occlusion shock (SAO). SAO shock was induced by clamping both the superior mesenteric artery and the celiac trunk, followed by release of the clamp. There was a marked increase in the peroxynitrite formation in the plasma of the SAO-shocked IL-6 wild-type (WT) mice after reperfusion. Immunohistochemical examination demonstrated a marked increase in the immunoreactivity to nitrotyrosine in the necrotic ileum in shocked IL-6 WT mice. SAO-shocked WT mice developed a significant increase of tissue myeloperoxidase (MPO) and malondialdehyde (MDA) activity and marked histological injury to the distal ileum. SAO shock was also associated with a significant mortality (0% survival). Reperfused ileum tissue sections from SAO-shocked WT mice showed positive staining for P-selectin. Little specific staining was observed in sham-WT mice. Staining of ileum tissue obtained from sham-operated WT mice with anti-ICAM-1 antibody showed weak but diffuse staining, demonstrating that ICAM-1 is constitutively expressed. However, after SAO shock the staining intensity increased substantially in the ileum section from WT mice. Intensity and degree of P-selectin and ICAM-1 were markedly reduced in tissue section from SAO-shocked IL-6 KO mice. SAO-shocked IL-6 KO mice also show significant reduction of neutrophil infiltration into the reperfused intestine, as evidenced by reduced MPO activity, improved histological status of the reperfused tissues, reduced peroxynitrite formation, reduced MDA levels, and improved survival. In vivo treatment with anti-IL-6 significantly prevents the inflammatory process. Our results clearly demonstrate that IL-6 plays an important role in ischemia and reperfusion injury and allows the hypothesis that inhibition of IL-6 may represent a novel and possible strategy. Part of this effect may be due to inhibition of the expression of adhesion molecules and subsequent reduction of neutrophil-mediated cellular injury. J. Leukoc. Biol. 66: 471–480; 1999.
Attenuated liver fibrosis and depressed serum albumin levels in carbon tetrachloride-treated IL-6-deficient mice
Authors: Natsume Miyoko , Tsuji Hirokazu , Harada Akihisa , Akiyama Mariko , Yano Tomoyuki , Ishikura Hiroshi , Nakanishi Isao , Matsushima Kouji , Kaneko Shu-ichi , Mukaida Naofumi 
Published: January 2018

Abstract
Chronic intermittent injection of carbon tetrachloride (CCI4) for more than 10 weeks induced liver fibrosis in mice, as evidenced by positive Azan staining and increased intrahepatic collagen content. Preceding the onset of liver fibrosis, interleukin-6 (IL-6) gene expression was enhanced in liver and immunoreactive IL-6 was detected in infiltrating inflammatory cells. To delineate the role of IL-6 in this process, we treated IL-6-deficient mice with CCl4 in a similar manner for 12 weeks, after which fibrotic changes were less evident and serum albumin levels were lower in IL-6-deficient than wild-type mice. Moreover, CCl4-induced expression of transforming growth factor β1 and hepatocyte growth factor genes in liver was significantly reduced in IL-6-deficient mice. Thus, IL-6 may be vitally involved in fibrotic changes and maintenance of serum albumin levels, partly by modulating intrahepatic expression of these cytokines. J. Leukoc. Biol. 66: 601–608; 1999.
A phagocytic challenge with IgG-coated erythrocytes depresses macrophage respiratory burst and phagocytic function by different mechanisms
Authors: Raley Michael J , Lennartz Michelle R , Loegering Daniel J 
Published: January 2018

Abstract
A phagocytic challenge with IgG-coated erythrocytes (EIgG) previously has been shown to cause impaired macrophage respiratory burst capacity and FcγR-mediated phagocytic function. Because both the respiratory burst and FcγR-mediated phagocytosis are dependent on the release of arachidonate (AA), we evaluated the effects of impaired AA release on the depression of macrophage function caused by a phagocytic challenge. Challenge with EIgG caused a depression of A23187-stimulated AA release that was associated with impaired phorbol myristate acetate (PMA)-stimulated H2O2 production and FcγR-mediated phagocytic function. In contrast, challenge with IgG-coated glass beads (BIgG) had no effect on either AA release or H2O2 production but did depress phagocytic function. Exogenous AA prevented the depression of H2O2 production but had no effect on phagocytic function. Phospholipase A2 (PLA2) activity was depressed under conditions where AA release was impaired. The depression of phagocytic function was correlated with a depression of both EIgG binding and FcγR expression. Thus, a phagocytic challenge with EIgG results in macrophage dysfunction by depressing PLA2 activity and depleting FcγR. J. Leukoc. Biol. 66: 803–808; 1999.
Internalization of FimH+ Escherichia coli by the human mast cell line (HMC-1 5C6) involves protein kinase C
Authors: Lin Tong-Jun , Gao Zhimin , Arock Michel , Abraham Soman N 
Published: January 2018

Abstract
Rodent mast cells (MC) play critical roles in host defense against bacterial infection. However, bacteria-mediated signaling mechanisms in MC have not been studied. In addition, the response of human MC to bacteria is not fully investigated. This study examined the interaction between human MC and type 1 fimbriated Escherichia coli and the mechanisms involved using the human MC line HMC-1 5C6 and human cord blood-derived MC. These MC internalized significant numbers of FimH+ E. coli, but not its isogenic FimH− mutant. In HMC-1 cells, bacterial internalization was stimulated by protein kinase C (PKC) activation [short-term phorbol myristate acetate (PMA) treatment] and dramatically decreased by PKC inhibitors or PKC depletion (long-term PMA treatment). Moreover, bacterial internalization was accompanied by significant expression of PKCβ1 and δ. Fluorescence microscopy demonstrated accumulation of PKCβ1 on internalized bacteria. These data indicate that human MC has the capacity to internalize bacteria and PKC may be a critical intracellular mediator of this function. J. Leukoc. Biol. 66: 1031–1038; 1999.
Regulation of intercellular adhesion molecule-1 (CD54) gene expression
Authors: Roebuck Kenneth A , Finnegan Alison 
Published: January 2018

Abstract
Intercellular adhesion molecule-1 (ICAM-1, CD54) is an inducible cell adhesion glycoprotein of the immunoglobulin supergene family expressed on the surface of a wide variety of cell types. ICAM-1 interactions with the β2 integrins CD11a/CD18 (LFA-1) and CD11b/CD18 (MAC-1) on the surface of leukocytes are important for their transendothelial migration to sites of inflammation and their function as costimulatory molecules for T cell activation. ICAM-1 is constitutively expressed on the cell surface and is up-regulated in response to a variety of inflammatory mediators, including proinflammatory cytokines, hormones, cellular stresses, and virus infection. These stimuli increase ICAM-1 expression primarily through activation of ICAM-1 gene transcription. During the past decade much has been learned about the cell type- and stimulus-specific transcription of ICAM-1. The architecture of the ICAM-1 promoter is complex, containing a large number of binding sites for inducible transcription factors, the most important of which is nuclear factor-kappa B (NF-κB). NF-κB acts in concert with other transcription factors and co-activators via specific protein-protein interactions, which facilitate the assembly of distinct stereo-specific transcription complexes on the ICAM-1 promoter. These transcription complexes presumably mediate the induction of ICAM-1 expression in different cell types and in response to different stimuli. In this review, we summarize our current understanding of ICAM-1 gene regulation with a particular emphasis on the transcription factors and signal transduction pathways critical for the cell type- and stimulus-specific activation of ICAM-1 gene transcription. J. Leukoc. Biol. 66: 876–888; 1999.
The tumorigenic and angiogenic effects of MGSA/GRO proteins in melanoma
Authors: Haghnegahdar Hamid , Du Jianguo , Wang DingZhi , Strieter Robert M , Burdick Marie D , Nanney Lillian B , Cardwell Nancy , Luan Jing , Shattuck-Brandt Rebecca , Richmond Ann 
Published: January 2018

Abstract
Continuous expression of the MGSA/GROα, β, or γ chemokine bestows tumor-forming capacity to the immortalized murine melanocyte cell line, melan-a. The mechanism for this transformation is unclear, although both autocrine and paracrine processes are possible because melan-a cells as well as endothelial cells express a low level of the receptor for this ligand. To further define the role of MGSA/GRO proteins in melanocyte transformation, two types of experiments were designed to neutralize the biological effects of MGSA/GRO in the transfected melan-a clones: (1) the effect of neutralizing antiserum to MGSA/GRO proteins on melan-a tumor growth was assessed; (2) the tumor-forming capacity of melan-a clones expressing ELR motif-mutated forms of MGSA/GRO with compromised receptor affinity was compared to the tumor-forming capacity of clones expressing wild-type MGSA/GRO. These experiments revealed that SCID mice inoculated with MGSA/GROα- or γ-expressing melan-a cells and subsequently treated with antiserum to the respective chemokine exhibited decreased tumor growth. This reduction in tumor growth was accompanied by declining angiogenic activity in MGSA/GROγ-expressing tumors. Moreover, athymic nude mice injected with melan-a cells expressing ELR-mutant forms of MGSA/GROα exhibited markedly impaired tumor-forming capacity compared with those mice injected with melan-a clones expressing wild-type MGSA/GRO. These data suggest that continuous expression of MGSA/GRO proteins may facilitate tumor growth by stimulating the growth of microvessels into the tumor (paracrine) and by affecting melanocyte growth (autocrine). J. Leukoc. Biol. 67: 53–62; 2000.
Langerhans cells acquire a CD8+ dendritic cell phenotype on maturation by CD40 ligation
Authors: Anjuere Fabienne , del Hoyo Gloria Martínez , Martín Pilar , Ardavín Carlos 
Published: January 2018

Abstract
Dendritic cell (DC) reconstitution experiments and phenotypic analysis of DC subpopu-lations have allowed the definition in the mouse of two main DC categories: CD8+ lymphoid DCs and CD8− myeloid DCs. With regard to Langerhans cells (LCs), which represent immature DCs differentiating into mature DCs on migration to the lymph nodes after an antigenic stimulation, although classically considered as myeloid DCs, there is no experimental evidence of their origin. It has been recently shown that mouse LCs, negative for CD8 and LFA-1, undergo CD8/LFA-1 up-regulation on migration, suggesting that LCs belong to the CD8+ lymphoid DC lineage. To further reinforce this hypothesis, we have analyzed the modulation of CD8 expression by LCs on culture with molecules known to induce LC maturation. Our results show that LC acquired a CD8+ lymphoid phenotype on CD40 ligation. J. Leukoc. Biol. 67: 206–209; 2000.
P47phox-deficient NADPH oxidase defect in neutrophils of diabetic mouse strains, C57BL/6J-m db/db and dbl+
Authors: Huang Chi-Kuang , Zhan Lijun , Hannigan Michael O , Ai Youxi , Leto Thomas L 
Published: January 2018

Abstract
Deficiencies in neutrophil NADPH oxidase proteins have been demonstrated in humans with chronic granulomatous disease. However, no spontaneous mutation in murine NADPH oxidase has been reported. In this study we report that neutrophils from the diabetic mouse strains, C57BL/6J-m heterozygous lean (leprdb/+) and homozygous obese (leprdb/db) mice produced no superoxide on stimulation. An absence of intact p47phox but not other oxidase proteins was observed in both mouse strains through the use of immunoblotting. Molecular analysis by reverse transcriptase-polymerase chain reaction identified three abnormal p47phox mRNA transcripts. Sequencing of genomic DNA of p47phox revealed a point mutation at the –2 position of exon 8, which is consistent with aberrant splicing of the p47phox transcript. These results indicate that the C57BL/6J-m db/db and db/+ mice are the first spontaneously derived murine model of NADPH oxidase deficiency involving a p47phox mutation. J. Leukoc. Biol. 67: 210–215; 2000.
Gender difference in cell-mediated immunity after thermal injury is mediated, in part, by elevated levels of interleukin-6
Authors: Gregory Meredith S , Faunce Douglas E , Duffner Lisa A , Kovacs Elizabeth J 
Published: January 2018

Abstract
The gender difference in normal immune function has been well documented, however, there is only limited information regarding whether such a difference occurs after injury. To investigate this, we examined cell-mediated immune responses in male and female mice given a 15% total body surface area dorsal scald or sham injury. Both delayed-type hypersensitivity (DTH) and splenocyte proliferative responses were significantly suppressed in males at 1 day and in females at 7 and 10 days post burn (P &lt; 0.01). The decreased splenocyte proliferation was found to be macrophagedependent and suppression of both immune parameters corresponded with elevated interleukin-6 (IL-6) levels. Furthermore, post-burn treatment with an anti-IL-6 antibody partially restored the DTH response in males at 1 day and females at 10 days post injury and completely restored splenocyte proliferation. These data demonstrate a possible mechanism for the gender difference in cell-mediated immune responses after thermal injury. J. Leukoc. Biol. 67: 319–326; 2000.
Differential regulation of TSG-14 expression in murine fibroblasts and peritoneal macrophages
Authors: Goodman Adam R , Levy David E , Reis Luiz F L , Vilçek Jan 
Published: January 2018

Abstract
Tumor necrosis factor (TNF)-stimulated gene 14 (TSG-14, also termed PTX3) encodes a secreted glycoprotein whose carboxyterminal half shares sequence similarity with the pentraxin family of acute phase proteins (C-reactive protein and serum amyloid P component). We compared TSG-14 mRNA expression in cultures of murine BALB/c 3T3 fibroblasts and thioglycollateelicited peritoneal macrophages. TNF and interleukin-1 (IL-1) potently induced TSG-14 expression in 3T3 fibroblasts but not in peritoneal macrophages. Lipopolysaccharide (LPS) elicited TSG-14 expression in both cell types, but induction in 3T3 cells and macrophages showed several distinct characteristics. Whereas in 3T3 fibroblasts TSG-14 mRNA was rapidly up-regulated by LPS, expression in macrophages was substantially delayed. Furthermore, cycloheximide greatly reduced LPS-induced TSG-14 mRNA up-regulation in macrophages but not in 3T3 cells. Finally, interferon-γ (IFN-γ; but not IFN-α/β) inhibited LPS-induced TSG-14 expression in macrophages and not in 3T3 fibroblasts. The antioxidant pyrrolidine dithiocarbamate inhibited LPS-induced nuclear factor-κB (NF-κB) activation and TSG-14 expression in macrophages. In contrast, IFN-γ did not inhibit NF-κB function as measured by IκB-α and IκB-β degradation, IκB-α resynthesis, or electrophoretic mobility shift analysis. Inhibition of LPS-induced TSG-14 mRNA expression by IFN-γ in macrophages was also observed in the presence of cycloheximide and in cells from STAT1 null mice, suggesting that IFN-γ inhibits TSG-14 expression through an unconventional mechanism. J. Leukoc. Biol. 67: 387–395; 2000.
Dexamethasone lowers cytosolic pH in macrophages by altering alkalinizing pH-regulatory mechanisms
Authors: Nauclér Claes , Sundler Roger , Tapper Hans 
Published: January 2018

Abstract
The effect of dexamethasone on cytosolic pH (pHc) in resident mouse peritoneal macrophages was investigated using the fluorescent probe 2′,7′-bis(carboxyethyl)-5(6)-carboxyfluorescein tetra-acetoxymethyl ester (BCECF-AM). Dexamethasone was found to significantly lower pHc and this reduction of pHc evolved gradually with time, was near maximal at 10 nM dexamethasone, and could be prevented by the glucocorticoid receptor antagonist RU-38486. The lower pHc of dexamethasone-treated cells was neither due to a reduction of cellular buffer capacity nor to an altered regulation of pHc by Na+/H+-exchange or by acidifying Na+-independent Cl−/HCO exchange, as assessed by studies of pH recovery after acute acid and alkali loads, respectively. Instead, an impaired pHc recovery by both the H+-ATPase and the alkalinizing Na+-dependent Cl−/HCO exchange was observed. This impairment was most likely not caused by an altered expression or localization of the 39-κDa subunit of the proton pump. Dexamethasone treatment caused a reduction of pHc also in a HCO-containing solution, suggesting that acid extrusion by both the H+-ATPase and Na+-dependent Cl−/HCO exchange is important for maintenance and regulation of macrophage resting pHc. The lowering of macrophage pHc might be one mechanism whereby glucocorticoids exert their anti-inflammatory effects. J. Leukoc. Biol. 67: 876–884; 2000.
Using Self‐Regulated Learning Strategies to Develop Students’ Multicultural Counseling Competency
Authors: Zeleke Waganesh A. , Karayiğit Cebrail , Myers‐Brooks Kaitlyn 
Published: January 2018

This study examines the effect of self‐regulated learning strategies on students’ multicultural competency development. Quantitative and qualitative data were collected from 26 students who took a semester‐long multicultural counseling course. Results show statistically significant improvement in students’ multicultural awareness and knowledge and statistical insignificance in multicultural skill development compared to their level of competence before the training. Implications of using this approach to teach multicultural counseling courses and future research are discussed.Este estudio examina el efecto de las estrategias de aprendizaje autorregulado en el desarrollo de la competencia multicultural de los estudiantes. Se recopilaron datos cuantitativos y cualitativos de 26 estudiantes que atendieron un curso de consejería multicultural de un semestre. Los resultados muestran una mejora estadísticamente significativa en la conciencia y conocimentos multiculturales de los estudiantes y una insignificancia estadística en el desarrollo de las habilidades multiculturales comparadas con su nivel de competencia antes de la capacitación. Se discuten las implicaciones de usar este enfoque didáctico en cursos de consejería multicultural y para investigaciones futuras.