bluuebunny/crossref_metadata_2025_split huggingface dataset:
Modulation of cellular annexin I in human leukocytes infiltrating DTH skin reactions
Authors: Perretti Mauro , Wheller Samantha K , Flower Roderick J , Wahid Smaira , Pitzalis Costantino 
Published: January 2018

Abstract
Based on our previous studies showing endogenous annexin I being depleted from migrated neutrophils (PMN) in vitro, we have tested whether the levels of this glucocorticoid-regulated protein in PMN and mononuclear cells (PBMC) were modified after adhesion to endothelial monolayers in vitro and extravasation into skin blisters in vivo. In vitro, annexin I levels were depleted more significantly (–70%) in post-adherent PMNs than in monocytes (–25%) and lymphocytes (–50%, only in the positive fraction). In vivo, a significant time-dependent increase (approximately threefold, P &lt; 0.05) in cell-associated annexin I was measured in PBMCs recovered from the blisters, whereas no significant changes were detected in extravasated PMNs. This was associated with annexin I release in the blister fluids (∼35 ng/mL), whereas no detectable protein was found in matched-paired plasmas. In conclusion, we report for the first time an activation of the annexin I pathway during an ongoing experimental inflammatory response in humans, which is differently regulated between PMNs and PBMCs. J. Leukoc. Biol. 65: 583–589; 1999.
Assessment of chemokine receptor expression by human Th1 and Th2 cells in vitro and in vivo
Authors: Annunziato Francesco , Cosmi Lorenzo , Galli Grazia , Beltrame Chiara , Romagnani Paola , Manetti Roberto , Romagnani Sergio , Maggi Enrico 
Published: January 2018

Abstract
The preferential association of some chemokine receptors with human Th1 or Th2 cells has recently been reported. In this study, the expression of CCR3, CCR5, CXCR3, and CXCR4 were analyzed by flow cytometry in three distinct in vitro models of Th1/Th2 polarization, activated naive and memory T cells, and T-cell clones, in which the intracellular synthesis of interferon-γ (IFN-γ) and interleukin-4 (IL-4) and the surface expression of CD30 and LAG-3 were also assessed. Moreover, by using immunohistochemistry the in vivo expression of CCR3, CCR5, CXCR3, and CXCR4 was examined in the gut of patients suffering from Crohn's disease, a Th1-dominated disorder, and in the skin of patients suffering from systemic sclerosis, a Th2-dominated disorder. CCR5 and LAG-3 exhibited the same pathway of Th1 association, whereas CXCR3 did not discriminate between Th1- and Th2-dominated responses. On the other hand, CCR3 was found only occasionally in a small proportion of allergen-specific memory T cells with Th2/Th0 profile of cytokine production in vitro. However, it was neither seen in Th2-polarized activated naive T cells nor in established Th2 clones and could be detected in vivo only on non-T cells. Finally, whereas CXCR4 expression was not limited to Th2 cells in vivo, it was markedly up-regulated by IL-4 and down-regulated by IFN-γ in vitro. Thus, the results of this study confirm the existence of flexible programs of chemokine receptor expression during the development of Th1 and Th2 cells. However, caution is advised in interpreting these receptors as surrogate markers of a given type of effector response. J. Leukoc. Biol. 65: 691–699; 1999.
Regulation of neutrophil FcγRIIIb (CD16) surface expression following delayed apoptosis in response to GM-CSF and sodium butyrate
Authors: Moulding Dale A , Hart C Anthony , Edwards Steven W 
Published: January 2018

Abstract
When neutrophils undergo apoptosis, they lose expression of the surface receptor CD16 (FcγRIIIb). Thus levels of surface CD16 are good indicators of apoptotic or non-apoptotic neutrophils. Shedding of CD16 occurs via the activity of a metalloproteinase that cleaves the receptor from the plasma membrane. Granulocyte-macrophage colony-stimulating factor (GM-CSF) and sodium butyrate both stimulate neutrophil gene expression, protect these cells from apoptosis, and maintain expression of surface CD16. In this report we have investigated whether these agents maintain surface expression of CD16 via (1) decreased shedding (2) increased mobilization of the internal pool of pre-formed CD16, or (3) via de novo biosynthesis of new receptor molecules. Although GM-CSF and sodium butyrate both preserved surface expression of CD16, GM-CSF actually accelerated the rate of shedding of this receptor. Maintenance of surface levels was achieved by substantial mobilization of the internal pool of CD16. Sodium butyrate, on the other hand, maintained surface expression without extensive store depletion via a mechanism that appeared to involve a decreased rate of shedding. In these experiments we could find no evidence for de novo biosynthesis of CD16 stimulated by either GM-CSF or sodium butyrate. These experiments indicate that multiple mechanisms exist for the maintenance of surface CD16 during rescue of neutrophils from apoptosis by different agents. J. Leukoc. Biol. 65: 875–882; 1999.
Functional studies on dendritic cells in the respiratory tract and related mucosal tissues
Authors: Holt P G , Stumbles P A , McWilliam A S 
Published: January 2018

Abstract
Recent reports indicate that mucosal tissues contain dendritic cell (DC) populations that exhibit phenotypic features distinct from those at more studied sites such as skin. In particular, mucosal DC populations display very rapid baseline turnover rates, which increase in response to local inflammatory stimuli. This property is likely to be central to the role of mucosal DC in surveillance of these front-line tissues for incoming microbial pathogens. As we discuss, it may also indirectly account for the “Th2 default,” which is the recognized hallmark of mucosal immune system in the steady state. J. Leukoc. Biol. 66: 272–275; 1999.
Differential responsiveness to constitutive vs. inducible chemokines of immature and mature mouse dendritic cells
Authors: Vecchi Annunciata , Massimiliano Lucia , Ramponi Simona , Luini Walter , Bernasconi Sergio , Bonecchi Raffaella , Allavena Paola , Parmentier Marc , Mantovani Alberto , Sozzani Silvano 
Published: January 2018

Abstract
Upon exposure to immune or inflammatory stimuli, dendritic cells (DC) migrate from peripheral tissues to lymphoid organs, where they present antigen. The molecular basis for the peculiar trafficking properties of DC is largely unknown. In this study, mouse DC were generated from CD34+ bone marrow precursors and cultured with granulocyte-macrophage-CSF and Flt3 ligand for 9 days. Chemokines active on immature DC include MIP1α, RANTES, MIP1β, MCP-1, MCP-3, and the constitutively expressed SDF1, MDC, and ELC. TNF-α-induced DC maturation caused reduction of migration to inducible chemokines (MIPIα, RANTES, MIP1β, MCP-1, and MCP-3) and increased migration to SDF1, MDC, and ELC. Similar results were obtained by CD40 ligation or culture in the presence of bacterial lipopolysaccharide. TNF-α down-regulated CC chemokine receptor (CCR)1, CCR2, and CCR5 and up-regulated CCR7 mRNA levels, in agreement with functional data. This study shows that selective responsiveness of mature and immature DC to inducible vs. constitutively produced chemokines can contribute to the regulated trafficking of DC. J. Leukoc. Biol. 66: 489–494; 1999.
Differential responses of human monocytes and macrophages to IL-4 and IL-13
Authors: Hart Prue H , Bonder Claudine S , Balogh Julianna , Dickensheets Harold L , Donnelly Raymond P , Finlay-Jones John J 
Published: January 2018

Abstract
The primary interleukin-4 (IL-4) receptor complex on monocytes (type I IL-4 receptor) includes the 140-kDa α chain (IL-4Rα) and the IL-2 receptor γ chain, γc, which heterodimerize for intracellular signaling, resulting in suppression of lipopolysaccharide (LPS)-inducible inflammatory mediator production. The activity of IL-13 on human monocytes is very similar to that of IL-4 because the predominant signaling chain (IL-4Rα) is common to both receptors. In fact, IL-4Rα with IL-13Rα1 is designated both as an IL-13 receptor and the type II IL-4 receptor. When the anti-inflammatory activities of IL-4 and IL-13 were investigated on synovial fluid macrophages and compared with the responses by monocytes isolated from the patients at the same time as joint drainage, the response profiles differed with some responses similar in the two cell populations, others reduced on the inflammatory cells. Similar differences were recorded in the response profiles to IL-4 and IL-13 by monocytes and monocytes cultured for 7 days in macrophage colony-stimulating factor (M-CSF) or granulocyte-macrophage CSF (GM-CSF) (monocyte-derived macrophages, MDMac). MDMac have reduced γc mRNA levels and reduced expression of the functional 64-kDa γc. There was a similar loss of IL-13Rα1 mRNA on monocyte differentiation. In turn, there was a significant reduction in the ability of IL-4 and IL-13 to activate STAT6. These findings suggest that different functional responses to IL-4 and IL-13 by human monocytes and macrophages may result from reduced expression of γc and IL-13Rα1. J. Leukoc. Biol. 66: 575–578; 1999.
Coexpression of binding sites for A(B) histo-blood group trisaccharides with galectin-3 and Lag antigen in human Langerhans cells
Authors: Smetana Karel , Holíková Zuzana , Klubal Radek , Bovin Nicolai V , Dvořánková Barbora , Bartůňková Jiřina , Liu Fu-Tong , Gabius Hans-Joachim 
Published: January 2018

Abstract
Galectin-3 is an immunomodulatory protein with binding capacity for various glycoconjugates including IgE. It has been shown to be produced by epidermal keratinocytes and is present on the surfaces of skin Langerhans cells (LC). Therefore, it may have a role in the pathogenesis of various skin diseases, such as atopic dermatitis. To study the expression of galectin-3 in LC, we used, in addition to specific antibodies, a panel of synthetic, carrier-immobilized, specific oligosaccharides of the A- and B-histo-blood group, which are recognized by this lectin. In the mean time, Birbeck granules were visualized with an anti-Lag antibody. The double labeling experiments showed a remarkable colocalization of signals for Lag antigen (Birbeck granules) and galectin-3, as well as the binding sites for A- and B-histo-blood group trisaccharides. The specificity of the oligosaccharide binding was demonstrated by the lack of binding by Lec, Led (H blood group antigen), and sLex, which are not recognized by galectin-3. These results suggest that galectin-3 is present in Birbeck granules, where it retains reactivity for its glycoligands. J. Leukoc. Biol. 66: 644–649; 1999.
Surface expression and rapid internalization of macrosialin (mouse CD68) on elicited mouse peritoneal macrophages
Authors: Kurushima H , Ramprasad M , Kondratenko N , Foster D M , Quehenberger O , Steinberg D 
Published: January 2018

Abstract
Macrosialin, the mouse homolog of human CD68, is a heavily glycosylated transmembrane protein found almost exclusively in macrophages. Its function remains uncertain. It has a high affinity for oxidized low-density lipoprotein (LDL) in ligand blots and antibodies against the human homolog, CD68, inhibit the binding of oxidized LDL to a human monocyte-derived cell line (THP-1). However, there is still controversy as to whether macrosialin, found predominantly in late endo-somes, is expressed at all on the plasma membrane. The present studies, done in thioglycollate-elicited peritoneal macrophages, confirm that macrosialin is predominantly intracellular but show clearly that 10–15% of it is expressed on the cell surface. Exchange with intracellular pools occurs at an extremely high rate. The results are compatible with a surface function, including internalization of bound ligands or adhesion to surfaces. J. Leukoc. Biol. 67: 104–108; 2000.
Extracellular matrix moieties, cytokines, and enzymes: dynamic effects on immune cell behavior and inflammation
Authors: Vaday Gayle G , Lider Ofer 
Published: January 2018

Abstract
Tissue injury caused by infection or physical damage evokes inflammatory reactions and events that are necessary for regaining homeostasis. Central to these events is the translocation of leukocytes, including monocytes, neutrophils, and T lymphocytes, from the vascular system, through endothelium, and into the extracellular matrix (ECM) surrounding the injured tissue. This transition from the vasculature into the site of inflammation elicits remarkable changes in leukocyte behavior as cells adhere to and migrate across ECM before carrying out their effector functions. Growing evidence suggests that, through its interactions with cytokines and degradative enzymes, the ECM microenvironment has a specialized role in providing intrinsic signals for coordinating leukocyte actions. Recent advances also reveal that enzymatic modifications to ECM moieties and cytokines induce distinctive cellular responses, and are likely part of the mechanism regulating the perpetuation or arrest of inflammation. This article reviews the findings that have elucidated the dynamic relationships among these factors and how they communicate with immune cells during inflammation. J. Leukoc. Biol. 67: 149–159; 2000.
Reduced brain edema after traumatic brain injury in mice deficient in P-selectin and intercellular adhesion molecule-1
Authors: Whalen Michael J , Carlos Timothy M , Dixon C Edward , Robichaud Paul , Clark Robert S B , Marion Donald W , Kochanek Patrick M 
Published: January 2018

Abstract
Platelet (P-) selectin and intercellular adhesion molecule-1 (ICAM-1) mediate accumulation of neutrophils in brain. However, the mechanisms regulating neutrophil accumulation and damage after traumatic brain injury (TBI) are poorly defined. We hypothesized that mice deficient in both P-selectin and ICAM-1 (-/–) would have decreased brain neutrophil accumulation and edema, and improved functional and histopathological outcome after TBI compared with wild-type (+/+). In Protocol I, neutrophils and brain water content were quantified at 24 h after TBI. No difference in brain neutrophil accumulation was observed between groups; however, brain edema was decreased in dual P-selectin and ICAM-1 –/– (P &lt; 0.05 vs. +/+ mice). In Protocol II, after TBI, tests of motor and memory function and histopathology were assessed over 21 days. No difference in motor or memory function or histopathological damage was observed between +/+ and –/– mice. A role for adhesion molecules in the pathogenesis of brain edema independent of leukocyte accumulation in brain is suggested. J. Leukoc. Biol. 67: 160–168; 2000.
Homing and adhesion molecules in autoimmune gastritis
Authors: Barrett Simon P , Riordon Amy , Toh Ban Hock , Gleeson Paul A , van Driel Ian R 
Published: January 2018

Abstract
The pathogenesis of autoimmune gastritis is the result of lymphocyte infiltration of the gastric mucosa, however, the events leading to the selective extravasation of autoreactive lymphocytes are unclear. Here we have examined the expression of adhesion molecules in the gastric mucosa of BALB/c mice with neonatal thymectomy-induced gastritis. The overall area of vascular endothelium was not significantly different between gastritic and non-gastritic mice. However, a significant increase in the area of mucosal endothelium expressing MAdCAM-1 in gastritic mice was observed. Treatment of neonatally thymectomized BALB/c mice with a MAdCAM-1 specific monoclonal antibody (MECA 367) reduced the incidence of autoimmune gastritis from 80 to 26%. Treatment with a monoclonal antibody (R1-2) directed to the MAdCAM-1 ligand, α44β7, also resulted in a reduction in the incidence of gastritis to 40%. These findings identify the α4β7/MAdCAM-I interaction as a pivotal event in the initiation of autoimmune gastritis. J. Leukoc. Biol. 67: 169–173; 2000.
Insights from mouse models of colitis
Authors: Boismenu Richard , Chen Yaping 
Published: January 2018

Abstract
Emerging studies using mouse models of experimental colitis are defining the nature of the immunological disturbances that initiate inflammation and destruction of the intestine. A better understanding of disease-promoting and -suppressing CD4+ T cells is providing insight into the mechanisms controlling immune responses within the intestinal compartment. Moreover, a role for distinct T cell populations, including intraepithelial γδT cells, in maintaining the physical integrity of the intestine was suggested by recent studies. Cytokine gene-knockout mice and anti-cytokine treatments remain important tools to define the pro- and anti-inflammatory functions of cytokines. These advances are fostering the design and evaluation of new therapeutic approaches that may eventually be applied to treat human inflammatory bowel disease. J. Leukoc. Biol. 67: 267–278; 2000.
Neurotransmitters of the sympathetic nerve terminal are powerful chemoattractants for monocytes
Authors: Straub Rainer H , Mayer Markus , Kreutz Marina , Leeb Sandra , Schölmerich Jürgen , Falk Werner 
Published: January 2018

Abstract
Macrophages in lymphoid organs are in close contact to nerve terminals of the sympathetic nervous system. Hence, these cells could be targets of neuronal modulation. We studied sympathetic neurotransmitters as chemoattractants enabling the aggregation of macrophages and nerve terminals. Norepinephrine (NE), neuropeptide Y (NPY), isoproterenol (β-adrenergic), p-aminoclonidine (α2-adrenergic), methoxamine (α1-adrenergic), and adenosine triphosphate (ATP) were used to study human monocyte and macrophage migration in 48-well Boyden chambers. NE stimulated chemotaxis of monocytes and macrophages at an optimal concentration of 10−10 M (P &lt; 0.025). Isoproterenol, but not p-aminoclonidine or methoxamine, induced chemotaxis of monocytes (10−10 M, P &lt; 0.05). In these studies, elevation of cAMP is a critical step in NE-induced chemotaxis of monocytes. NPY (10−11 M, P &lt; 0.05) stimulated monocyte chemotaxis as well. ATP at 10−4 and 10−5 M stimulated undirected cell mobility (P &lt; 0.05). All tested neurotransmitters of the sympathetic nerve terminal were potent chemoattractants. These findings may explain the close association of nerves and macrophages in tissue and lymphoid organs and may thus be of functional relevance in neuroimmunomodulation. J. Leukoc. Biol. 67: 553–558; 2000.
Analysis of interferon-γ-dependent and -independent pathways of macrophage activation
Authors: Paulnock Donna M , Demick Karen P , Coller Susan P 
Published: January 2018

Abstract
Macrophages are a cellular cornerstone of the innate immune response. The outcome of macrophage activity during development of an immune response to microbes results from macrophage activation by both organism-derived and host-derived factors. In order to more fully understand the spectrum of responses expressed by macrophages when encountering these distinct stimuli, we investigated the similarities and differences between interferon-γ receptor (IFN-γR)dependent macrophage activation and stimulation of macrophages through the Type A1 scavenger receptor (SR). We observed distinct patterns of macrophage activation depending on the nature of the ligand. IFN-γ and the SR ligand lipotechoic acid (LTA) induced largely non-overlapping sets of genes. The use of two additional SR ligands, maleylated bovine serum albumin and the polydeoxynucleo-tide poly dI:dC, revealed differences within SR activation-induced gene expression. We also observed that priming with IFN-γ resulted in an enhanced response to subsequent SR-mediated activation. These results suggest that full potentiation of macrophage activity during development of an antimicrobial immune response is achieved by activation of these cells through multiple receptors. J. Leukoc. Biol. 67: 677–682; 2000.
Coordinate activation of endogenous p38a, β, γ, and δ by inflammatory stimuli
Authors: Fearns C , Kline L , Gram H , Di Padova F , Zurini M , Han J , Ulevitch R J 
Published: January 2018

Abstract
The p38 family of mitogen-activated protein kinases is believed to mediate a variety of leukocyte responses to pro-inflammatory stimuli. There are four members of the p38 family, and although activation of the different members has been studied in transiently transfected cells much less is known about activation of the endogenous p38s, particularly in myeloid lineage cells. To investigate activation of endogenous p38s, we have made monoclonal antibodies specific for each p38 and have used these antibodies to study p38 activation by pro-inflammatory stimuli in several human monocytic cell lines. Without stimulation endogenous p38α kinase activity was readily detectable, whereas that of p38β, γ, and δ was barely measurable. In response to inflammatory stimuli, we observed a time- and dose-dependent activation of all four p38s. The kinetics of activation of each of the p38s were similar for each stimulus used, suggesting a common upstream activation pathway. Simultaneous activation of the p38s suggests that all four may be important in inflammation. J. Leukoc. Biol. 67: 705–711; 2000.
A molecular analysis of NKT cells: identification of a class-I restricted T cell-associated molecule (CRTAM)
Authors: Kennedy Jacqueline , Vicari Alain P , Saylor Vicki , Zurawski Sandra M , Copeland Neal G , Gilbert Debra J , Jenkins Nancy A , Zlotnik Albert 
Published: January 2018

Abstract
cDNA library subtraction techniques were used to identify transcripts expressed by activated mouse αβPTCR+ CD4−CD8− (double-negative; DN) T cells, a subset of natural killer T (NKT) cells. The most frequent cDNAs identified included the chemokines TCA3, macrophage inflammatory protein-1α (MIP-1α), MIP-1β, and lymphotactin (LPTN), the cytokines interleukin-4 (IL-4) and interferon-γ (IFN-γ), and a granzyme. We also identified a new member of the immunoglobulin superfamily (Ig-SF). This molecule was designated class I-restricted T cell-associated molecule (CRTAM) as a result of its restricted expression pattern in T cells. Human CRTAM was also identified, and shares the same expression pattern as the mouse molecule. LPTN and CRTAM exhibit the same expression pattern in T cells, suggesting the existence of a gene expression program common to class I-MHC-restricted T cells. J. Leukoc. Biol. 67: 725–734; 2000.
Hypoxemia modifies circulating and exudate neutrophil number and functional responses in carrageenin-induced pleurisy in the rat
Authors: Tremblay Pierre-Benoît , Macari David MT , Martel Dominique , du Souich Patrick , Barja-Fidalgo Christina , Marleau Sylvie 
Published: January 2018

Abstract
To assess the effect of hypoxemia on the responses of polymorphonuclear neutrophils (PMN) during an inflammatory response, rats were maintained in a low FiO2 atmosphere (9% O2) or room air for 12 h before intrathoracic injection of carrageenin or intradermal injections of agonists. After 4 h, hypoxemic rats had 50% more circulating PMN in blood and 25% less PMN in pleural exudate, whereas the number of PMN in skin biopsies did not differ from controls. Following hypoxemia, basal adhesion of blood PMN to serum-coated plastic wells was unchanged, whereas fMLP-stimulated adhesion was 50% greater. In contrast, basal adhesion of exudate PMN was 72% greater. In hypoxemic rats, exudate PMN produced 64% more PMA-stimulated superoxide than blood PMN; furthermore, blood and exudate PMN produced 4.5- and 2-fold more LPS-stimulated nitric oxide than controls, respectively. These results show that a moderate level of hypoxemia may trigger mechanisms that will interfere with PMN emigration yet prime these cells for enhanced responses upon stimulation. J. Leukoc. Biol. 67: 785–792; 2000.