bluuebunny/crossref_metadata_2025_split huggingface dataset:
Human blood dendritic cells: binding to vascular endothelium and expression of adhesion molecules
Authors: BROWN K A , BEDFORD P , MACEY M , MCCARTHY D A , LEROY F , VORA A J , STAGG A J , DUMONDE D C , KNIGHT S C 
Published: November 2003

SUMMARY
To investigate the binding properties of dendritic cells (DC) to vascular endothelium, a comparative analysis was undertaken of DC, monocytes and lymphocytes isolated from the blood of 25 healthy subjects using monolayers of human umbilical vein endothelial cells as the adherence substrate. More blood DC (mean 24% adherence) were adherent to endothelial monolayers than monocytes (mean 18%; P &lt; 0.001) and lymphocytes (mean 12%; P &lt; 0.001). When the monolayers were pretreated with tumour necrosis factor-alpha (TNF-α) all leucocyte populations exhibited an increased attachment, but there was still greater binding of DC (mean 37% adherence) in comparison with monocytes (mean 23%; P &lt; 0.001) and lymphocytes (mean 18%; P &lt; 0.001). Flow cytometric analysis revealed that in relation to monocytes and lymphocytes the DC had a higher surface expression of the adhesion molecules CD11a (P &lt; 0.05), CD11c (P &lt; 0.05) and CD54 (P &lt; 0.05) but a lower prevalence of cells bearing CD49d (mean 38%; P &lt; 0.05) and the homing receptor CD62L (mean 14%; P &lt; 0.001). CD1a was present on 22% of DC and virtually absent from the surface of monocytes and lymphocytes. The intensity of expression of the β1-integrins, CD49c, CD49d and CD49e was greater on DC than lymphocytes and monocytes (P &lt; 0.05). Antibody blocking studies demonstrated that DC binding to untreated and TNF-α-treated endothelium was dependent upon the expression of CD11a, CD18 and CD49d, and the simultaneous application of anti-CD18 and anti-CD49d antibodies produced an approximate 70% inhibition of adhesion (P &lt; 0.001). Thus, the expression of both β1- and β2-integrins contributes to the adhesive interaction between DC and endothelium.
Up-regulation of the granulocyte adhesion molecule Mac-1 by autoantibodies in autoimmune vasculitis
Authors: Johnson P A , Alexander H D , McMillan S A , Maxwell A P 
Published: November 2003

SUMMARY
The characteristic finding of autoantibodies in patients with vasculitis has raised the possibility that these antibodies play a role in the pathogenesis of the disease. The expression of adhesion molecules (AM) on leucocytes and endothelial cells is believed to be integral to the development of vasculitis. We therefore investigated the effect of sera, positive for anti-neutrophil cytoplasmic antibodies (ANCA) or anti-nuclear antibodies (ANA) from patients with vasculitis, on granulocyte expression of the adhesion molecule Mac-1 (CD11b). Autoantibody-positive sera from 15 out of 35 patients with vasculitis stimulated an up-regulation of Mac-1 on granulocytes. In most cases this effect was reproduced by the autoantibody-positive purified IgG fraction. Autoantibody-negative samples did not stimulate AM up-regulation. Of interest, preincubation of sera with purified antigens did not inhibit AM up-regulation by the autoantibody samples. Blocking the Fc receptors on granulocytes did result in a decrease of Mac-1 up-regulation, but this trend was not statistically significant. These results suggest that both ANCA and ANA have the capacity to up-regulate granulocyte AM expression, and that while Fc interaction with granulocyte Fc receptors is important, it is not the only mechanism whereby such autoantibodies activate cells.
VH genes expressed in peripheral blood IgE-producing B cells from patients with atopic dermatitis
Authors: TILGNER J , GOLEMBOWSKI S , KERSTEN B , STERRY W , JAHN S 
Published: November 2003

SUMMARY
In this study we analysed the VH genes expressed in IgE-producing peripheral B cells in two patients with severe atopic dermatitis. We found a diverse antibody repertoire containing VH genes of five different VH families, no VH2 and 7 genes, with no biased usage of one particular VH gene family. Some VH germ-line segments were found to be used several times within the ε transcripts (V3–23, V3–30). Comparison of the IgE-encoding VH genes with the respective germ-line elements revealed the expression of nearly germ-line identical as well as somatically mutated VH genes. In these latter VH genes base substitutions were distributed over both complementarity determining and framework regions. Because of the similarities between the IgE committed B cell repertoire in atopic patients and the peripheral B cell repertoire in non-atopic individuals we conclude that the atopic VH gene repertoire probably reflects the result of an increased class switch of polyclonal B cells, including virgin and mature B cells, in response to a Th2 cytokine profile.
A distinct pattern of cytokine production from blood mononuclear cells in multitransfused patients with β-thalassaemia
Authors: SALSAA B , ZOUMBOS N C 
Published: November 2003

SUMMARY
The unstimulated and induced production of granulocyte-macrophage colony-stimulating factor (GM-CSF), granulocyte colony-stimulating factor (G-CSF), IL-3, IL-6, stem cell factor (SCF), IL-1β, tumour necrosis factor-alpha (TNF-α), TNF-β, interferon-gamma (IFN-γ) and transforming growth factor-beta (TGF-β) was determined after culture of blood mononuclear cells from 22 patients with severe β-thalassaemia in a regular transfusion programme, five non-regularly transfused patients with β-thalassaemia intermedia and nine normal persons. A distinct pattern of cytokine production in thalassaemic patients was detected, namely a low unstimulated production of all cytokines and a significant increase in the stimulated production of IFN-γ, TNF-α and IL-1β; these abnormalities were more pronounced in the more heavily transfused older patients. The increased production of the above cytokines, which usually characterize the acute response to infectious agents and have a negative effect on erythropoiesis, may explain the deterioration of anaemia found in thalassaemic patients during acute infections.
CD44 and hyaluronan expression in the development of experimental crescentic glomerulonephritis
Authors: JUN Z , HILL P A , LAN H Y , FOTI R , MU W , ATKINS R C , NIKOLIC-PATERSON D J 
Published: November 2003

SUMMARY
CD44 is a widely expressed cell surface glycoprotein which is involved in both cell–matrix and cell–cell interactions which regulate a variety of processes, including leucocyte migration and activation. Therefore, we examined the expression of CD44, and its major ligand hyaluronan, during the induction and progression of experimental glomerulonephritis. Antibody staining of normal rat kidney showed constitutive CD44 expression by resident glomerular macrophages, parietal epithelial cells, medullary and occasional cortical tubules. There was a marked increase in CD44 expression over days 1, 7 and 21 of rat crescentic anti-glomerular basement membrane (GBM) glomerulonephritis. Infiltrating monocytes and lymphocytes were CD44+, with ultrastructural studies showing high levels of CD44 expressed on the surface of lymphocytes adherent to activated endothelium. Marked hyaluronan deposition was seen in areas of fibrosis on days 7 and 21, such as glomerular crescents and the periglomerular area. Hyaluronan deposition was accompanied by the presence of many CD44+ cells. Double immunohistochemistry showed that both CD44+ED1+ macrophages and CD44+ myofibroblasts (identified by expression of α-smooth muscle actin) were present in areas of fibrosis. There was also a dramatic increase in cortical tubular CD44 expression, which was most evident in areas of tubular damage. Although tubular epithelial cells expressed CD44 upon both the basolateral and luminal surface, CD44 expression was most prominent within tight junctions, suggesting a role for CD44–CD44 interactions in cell–cell adhesion within the tubule. Analysis of CD44 isoforms by reverse transcriptase-polymerase chain reaction (RT-PCR) showed that the standard form of CD44 predominated in both normal and diseased kidney. However, a series of alternatively spliced CD44 isoforms was also detected, whose expression was markedly increased during disease. At least seven isoforms containing the v6 domain were identified, with the smallest form representing activated T cells. In conclusion, CD44 is constitutively expressed in normal kidney and is dramatically up-regulated in rat anti-GBM disease, suggesting possible roles for the CD44–hyaluronan interaction in leucocyte recruitment, renal fibrosis and tubular cell–matrix and cell–cell interactions during the induction and progression of crescentic glomerulonephritis.
Further study on the roles of the effector molecules of immunosuppressive macrophages induced by mycobacterial infection in expression of their suppressor function against mitogen-stimulated T cell proliferation
Authors: MAW W W , SHIMIZU T , SATO K , TOMIOKA H 
Published: November 2003

SUMMARY
Previously, we found that phospholipids and reactive nitrogen intermediates (RNI) collaborated in expression of the T cell mitogenesis-inhibitory activity of immunosuppressive macrophages induced by Mycobacterium avium-intracellulare complex (MAIC) infection. In this study, we examined the roles of free fatty acids (FFA) and prostaglandins (PG) as effectors of MAIC-induced macrophages, and moreover, their collaborating effects with RNI. First, treatment of MAIC-induced macrophages with quinacrine (phospholipase A2 (PLA2) inhibitor), dexamethasone (inhibitor of PLA2 and PG synthesis) or indomethacin (PG synthesis inhibitor) attenuated their suppressor activity against concanavalin A (Con A)-induced mitogenesis of splenocytes (SPC), indicating important roles of FFA liberated from membrane phospholipids and PG, as effectors. Second, oleic acid, PGE2, RNI generated from NOR 4 (a new nitric oxide (NO) donor), and phosphatidylserine (PS) exhibited suppressor activity against SPC mitogenesis without showing significant cytotoxicity, in an irreversible manner. Third, the suppressor activities of RNI and PGE2 were potentiated by combined use with oleic acid in a synergistic manner. Fourth, a dual-chamber experiment in which target SPC were separated from MAIC-induced macrophages by a Millipore filter revealed a requirement for cell-to-cell contact for expression of the suppressor function of MAIC-induced macrophages. These findings indicate that RNI, FFA, PG, and phospholipids (presumably PS) and their collaboration play central roles in expression of the T cell mitogenesis-inhibitory function of MAIC-induced suppressor macrophages.
Lymphocyte activation and subset redistribution in the peripheral blood in acute malaria illness: distinct γδ+ T cell patterns in Plasmodium falciparum and P. vivax infections
Authors: WORKU S , BJÖRKMAN A , TROYE-BLOMBERG M , JEMANEH L , FÄRNERT A , CHRISTENSSON B 
Published: November 2003

SUMMARY
Lymphocyte subset distributions and activation in the peripheral blood were studied in 39 patients with acute malaria and 16 healthy controls from Addis Ababa and Nazareth, Ethiopia. As confirmed by polymerase chain reaction (PCR), 15 patients were infected with Plasmodium falciparum (Pf ), 17 with P. vivax (Pv) and seven were double-infected (Di) with both Pf and Pv. Three-colour flow cytometry was used for phenotyping. Total leucocyte and lymphocyte counts were lower in malaria patients than in controls. The T cell count was reduced in Pf patients, while in the Pv and Di patients there was a reduction in the natural killer (NK) cell count. The CD4/CD8 ratio remained unchanged. γδ+ T cells were significantly elevated in Pf and Di patients, but not in Pv patients. The increase in γδ+ T cells was mostly due to an increase in Vδ1+ cells. Analyses of cellular activation indicated by the expressions of CD25 and HLA-DR revealed significantly higher numbers of activated CD3+ cells, including γδ+ T cells, in all patient groups compared with controls. Our results thus indicate that in acute malaria illness there is a complex pattern of change in lymphocyte subset distribution and activation, including γδ+ T cells. These patterns in Pf infection seem to be distinct from those in Pv infection.
IgE epitope analysis of the hevein preprotein; a major latex allergen
Authors: BEEZHOLD D H , KOSTYAL D A , SUSSMAN G L 
Published: November 2003

SUMMARY
We have previously identified the hevein preprotein as a common allergen for latex allergic healthcare workers. The B cell epitopes in the hevein protein that are recognized by IgE of latex-allergic individuals have not been identified. In this study, we examined the hevein preprotein using epitope mapping. Overlapping synthetic peptides of 10 amino acids (two aa overlap) were synthesized on a derivatized cellulose membrane using Fmoc chemistry. The peptide spots were probed with pooled sera from 10 latex-allergic patients, and the IgE-reactive peptides identified with anti-IgE MoAbs. We identified six B cell epitopes within the full length hevein preprotein which bound IgE from latex-allergic patients. Two were located in the N-terminal 5-kD hevein domain and four were observed in the 14-kD C-domain. A broad epitope was located between the N-terminal amino acids 13–24. This epitope had nearly complete homology to wheat germ agglutinin (WGA). Immunological cross-reactivity to WGA was confirmed by Western blot analysis with purified WGA, and this reactivity could be inhibited by latex proteins or WGA. Of the five remaining epitopes, four had homologies to other proteins in the pathogenesis-related family of plant proteins (PR-4). The data demonstrate that hevein has multiple IgE epitopes. The significant homology of these epitopes to a broad family of plant defence proteins further explains the increased prevalence of food allergies in latex-allergic individuals.
Up-regulation of IL-8 secretion by alveolar macrophages from patients with fibrosing alveolitis: a subpopulation analysis
Authors: PANTELIDIS P , SOUTHCOTT A M , BLACK C M , DU BOIS R M 
Published: November 2003

SUMMARY
Neutrophil accumulation in the lower respiratory tract of patients with fibrosing alveolitis is thought to be facilitated by IL-8, a neutrophil chemoattractant primarily secreted by mononuclear phagocytes. The aims of this study were: (i) to explore IL-8 secretion by lung and blood mononuclear phagocytes in subjects with cryptogenic fibrosing alveolitis, systemic sclerosis with and without fibrosing alveolitis, sarcoidosis and normal individuals; (ii) to examine IL-8 secretory heterogeneity in alveolar macrophages and peripheral blood monocytes; and (iii) to correlate alveolar macrophage phenotypic profile to IL-8 secretion. We observed that more monocytes secreted IL-8 than autologous macrophages and that there was heterogeneity in the in vitro IL-8 secretion by alveolar macrophages and peripheral blood monocytes. IL-8 secretion by alveolar macrophages was significantly higher in subjects with fibrosing alveolitis compared with subjects without fibrosing alveolitis, due to a higher percentage of IL-8-secreting alveolar macrophages in the fibrotic group both in the absence (P&lt;0.002) and presence of lipopolysaccharide (LPS) (P&lt;0.04) and correlated with bronchoalveolar lavage neutrophil percentage. Using the MoAbs RFD1, RFD7 and RFD9, that distinguish subsets of alveolar macrophages, we have been able to identify associations between secretion of IL-8 and smaller cells and the cells identified by the MoAb RFD7. In situ hybridization of the bronchoalveolar lavage cell population revealed that alveolar macrophages are the predominant source of IL-8 in the lung. We conclude that there is an increased number of IL-8-secreting alveolar macrophages in the lungs of patients with fibrosing alveolitis, and IL-8 secretion by these cells is associated with specific phenotypic profile expression.
Coordinate expression of group II phospholipase A2 and the acute-phase proteins haptoglobin (HP) and α1-anti-chymotrypsin (ACH) by HepG2 cells
Authors: VADAS P , GROUIX B , STEFANSKI E , WLOCH M , PRUZANSKI W , SCHROEDER J , GAULDIE J 
Published: November 2003

SUMMARY
The early response to inflammation is characterized by the synthesis of a variety of proteins under cytokine and glucocorticoid control. During episodes of infection or inflammation, a secretory phospholipase A2 (sPLA2) appears in the circulation along with a variety of acute-phase proteins (APP), suggesting possible common regulatory elements amongst sPLA2 and APP. Using the human hepatoma line, HepG2, regulation of sPLA2 expression was examined in relation to synthesis of HP and ACH. The patterns of induction of sPLA2, HP and ACH were distinct for each of IL-1, tumour necrosis factor (TNF) and IL-6, oncostatin M, IL-11 and leukaemia inhibitory factor. Dexamethasone had an enhancing effect on IL-6-induced expression of HP and ACH, but inhibited sPLA2 expression by 50%. Both 8-bromo-cAMP and dibutyryl cAMP increased sPLA2 expression (48.8-fold and 64.2-fold, respectively), whereas KT5720, an inhibitor of protein kinase A, down-regulated cytokine-induced sPLA2 synthesis by 51%. These data show that a panel of cytokines induced varying patterns of up-regulation of sPLA2, ACH and HP. Although dexamethasone potentiated IL-6-induced APP expression in HepG2 cells, it suppressed sPLA2 expression in a dose-dependent manner. In several respects, sPLA2 regulation is similar to that of HP and ACH, but a notable difference is the reciprocal effect of glucocorticoids on sPLA2 expression compared with that of ACH and HP.
Binding and inhibition of myeloperoxidase (MPO): a major function of ceruloplasmin?
Authors: SEGELMARK M , PERSSON B , HELLMARK T , WIESLANDER J 
Published: November 2003

Summary
Interactions between plasma proteins and MPO were studied. The protein fraction of normal plasma and serum was shown to exhibit an inhibitory effect on the peroxidase activity of MPO. Most of the inhibitory effect could be retained on an MPO-coupled affinity chromatography column. In particular, a protein with apparent mol. wt of 130 kD showed affinity for MPO. The protein was identified as ceruloplasmin by N-terminal amino acid sequencing and immunochemistry. During separation procedures the peroxidase inhibitory effect was limited to ceruloplasmin-containing fractions of plasma. Purified ceruloplasmin inhibited the peroxidase activity of MPO in a concentration-dependent manner, and exhibited selective binding to MPO-coated microtitre plates. This binding could be inhibited by MPO dissolved in buffer. Correspondingly the binding of MPO to ceruloplasmin-coated plates could be blocked by ceruloplasmin in solution, showing a physical interaction to occur between the two proteins under physiological conditions. We also found affinity to exist between MPO and C3 (and its C3d-containing fragments). However, C3 and C3 fragments did not inhibit the peroxidase reaction in vitro. We propose that ceruloplasmin takes part in the clearance and inactivation of MPO, in vivo. We also speculate that impaired inactivation of MPO may have a pathophysiological role in inflammatory diseases characterized by autoantibodies to MPO, such as rapidly progressive glomerulonephritis with P-ANCA (perinuclear anti-neutrophil cytoplasmic antibodies).
The influence of allotypes on the IgG subclass response to chromosomal β-lactamase of Pseudomonas aeruginosa in cystic fibrosis patients
Authors: CIOFU O , PRESSLER T , PANDEY J P , HØIBY N 
Published: November 2003

SUMMARY
Sera from 70 adult cystic fibrosis (CF) patients with chronic lung infection with Pseudomonas aeruginosa were typed for seven GM and two KM allotype determinants. IgG class and all four IgG subclasses of antibodies against chromosomal β-lactamase of Ps. aeruginosa (aβab) were measured in all 70 CF patients in a cross-sectional study. The aβab IgG subclass response in sera collected during the first 11 years of chronic infection from 20 CF patients (10 patients with G3M*5 G1M*3/G3M*5 G1M*3 genotype and 10 patients with G3M*21 G1M*1/G3M*21 G1M*1 genotype) was analysed in a longitudinal study. Increased levels of IgG2 were associated with the presence of GM 23 allotype. IgG3 aβab levels were the lowest for subjects with the GM 1,2,3,17 23 5,21 and GM 1,3,17 21 phenotypes and the highest in subjects with GM 3,23,5 and GM 3,5. No significant differences in IgG1 and IgG4 aβab levels were found between the different phenotypes. IgG1 aβab levels were higher in patients with KM*3/KM*3 genotype compared with patients with KM*3, *1 genotype. Patients with G3M*5 G1M*3/G3M*5 G1M*3 genotype had in both the cross-sectional and the longitudinal study higher IgG3 aβab, lower IgG4 aβab levels and poorer lung function than patients with G3M*21 G1M*1/G3M*21 G1M*1 genotype. An influence of the allotypes on the clinical course of chronic lung infection with Ps. aeruginosa in patients with CF is suggested.
Measles virus induces apoptotic cell death in lymphocytes activated with phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore
Authors: ITO M , WATANABE M , IHARA T , KAMIYA H , SAKURAI M 
Published: November 2003

SUMMARY
Peripheral blood mononuclear cells (PBMC) and T lymphocytes were infected with measles virus (MV) and cultured with a protein kinase C (PKC) activator, PMA and a calcium ionophore, ionomycin. After stimulation, cell viability and incorporation of 5-bromo-2′-deoxyuridine (BrdU) were decreased in MV-infected cells compared with mock-infected cells. DNA content analysis and terminal deoxytransferase (TdT)-mediated dUTP nick end labelling demonstrated that the hypodiploid fraction and DNA fragmentation were increased in MV-infected, T lymphocytes activated with PMA plus ionomycin. These data suggest that MV induces apoptotic cell death in cells activated by PMA plus ionomycin. In contrast to stimulation with PMA plus ionomycin, mitogenic stimulation with phytohaemagglutinin (PHA) did not induce apoptotic cell death in MV-infected cells, although cell proliferation was suppressed. Apoptosis induced in stimulated, MV-infected cells may be one mechanism of immunosuppression.