bluuebunny/crossref_metadata_2025_split huggingface dataset:
LAM-1/Leu 8 antigen is expressed on portal, but not on tabular intrahepatic mononuclear cells in inflammatory liver disease
Authors: VOLPES R , VAN DEN OORD J J , DESMET V J 
Published: July 2010

SUMMARYThe expression of the selectin receptor LAM-1/Lcu 8 was analysed in normal and in inflamed liver tissue, and its expression on mononuclear inflammatory cells was correlated with their topographical distribution in various compartments of the inflamed liver, in order to obtain new insights on possible molecular mechanisms involved in the traffic of mononuclear inflammatory cells throughout the diseased hepatic parenchyma. In normal liver tissue, few scattered mononuclear cells in portal and lobular parenchyma corresponded to both CD4+ and CD8+, as well as to CD45RA+ (2H4+) naive and CD45RO+ (UCHL1 +) memory T cells, and were LAM-1 /Leu 8+. In acute and chronic inflamed liver biopsies. CD45RO+ (UCHL1 +)CD4+ and CD8+ memory T cells largely predominated in both portal and lobular parenchyma. The expression of LAM- 1/Leu 8 antigen on these memory T cells varied according to their localization in the liver parenchyma, and it was not correlated with specific aetiological causes. In acute hepatitis, the vast majority of T lymphocytes were LAM-1/Leu 8. In chronic active hepatitis, memory T cells in portal tracts expressed LAM-1 /Leu 8. whereas virtually all intralobular T cells accumulating in areas of periportal and intralobular inflammation were LAM-1/ Leu 8. In chronic persistent hepatitis, the LAM-1/Leu 8+ T cells largely predominated among the numerous mononuclear inflammatory cells within enlarged portal tracts, whereas LAM-1/Leu 8 T cells were restricted to areas of intralobular ‘spotty’ inflammation. Therefore, two phenotypical populations can be recognized among the memory T cells in inflamed liver tissue, according to their topographical localization: LAM-1/Leu 8+ Tcells predominating in portal tracts, and LAM-1/Leu 8 T cells predominating in the lobular parenchyma. These data show that during their migration through the inflamed liver parenchyma, memory T lymphocytes undergo phenotyical changes (LAM-1/Leu 8 shedding) according to their localization in different liver compartments (portal tracts vs. lobular parenchyma), suggesting multiple cellular and molecular mechanisms involved in the regulation of the leucocyte traffic through inflamed liver tissue.
Repertoire of CDS+ and CD5− cord blood B cells: specificity and expression of VH I and VH III associated idiotopes
Authors: MACKENZIE L E , MAGEED R A , YOUINOU P Y , YUKSEL B , JEFFERIS R , LYDYARD P M 
Published: July 2010

SUMMARYEpstein-Barr (EBV)-immorlalized B cell clones were established from CD5+ and CD5 cord blood B cells separated by flow cytometry. We have previously shown that lgM from many of the clones was polyreacti ve, exhibiting reactivity with a number of autoantigens. In this study, IgM produced by the clones was analysed by MoAb for the expression of cross-reactive idiotypes (CRI) associated with rheumatoid factor paraproteins and from defined VH and Vk subgroups of immunoglobulin heavy and light chains. IgM produced by clones established from CD5+ and CDS B cells expressed the VH I associated idiotope G8. Furthermore, IgM produced by both sets of clones exhibited a similar frequency of VH III heavy chain subgroup expression, as determined by reactivity with staphylo-coccal protein A (SpA) and VH III-associated CRI expression (B6 and/or DI2). In contrast, expression of the V, III-associated 17.109 CRI was significantly higher in IgM antibodies produced by clones established from CD5+ compared with the CD5– clones(32 versus 5%: P &lt; 0·05). Analysis of the VH and VL subgroup expression by IgM produced by the CD5’ and CD5 cord blood clones, and their autoantigen reactivity profile did not reveal restriction or selection within CD5+ and CD5–populations. However, our data suggest that differences may exist in the expression of certain germline genes between CD5+ and CD5– cord blood B cells and might indicate an expansion of CD5+ B cells within the fetal environment.
Modulation of human T cell functions by surface sulphydryl groups: differential effects on IL-2 production and responsiveness
Authors: SMITH S , BROWN-GALATOLA C H , HALL N D 
Published: July 2010

SUMMARYAn impermeable thiol blocker has been used to investigate the role of sulphydryl (SH) groups in the production of and responsiveness to IL-2 by normal human T lymphocytes. Surface SH blockade of mononuclear cells prior to incubation with mitogen (phytohaemagglutinin, concanavalin A, CD3 MoAb) had no effect on production of IL-2 but markedly impaired cellular responsiveness to exogenous IL-2. Studies using MoAbs indicated that this effect was accompanied by decreased expression of both the CD25 and p75 subunits of the IL-2 receptor. Blocking surface SH groups did not affect binding of IL-2 to p75 on unstimulated mononuclcar cells, but inhibited binding to high-affinity receptors on a T lymphoma cell line. The data are consistent with the hypothesis that sulphydryl groups on the IL-2 receptor are required for its function and may be involved in the interaction of the CD25 and p75 subunits leading to generation of the high-affinity binding site. The surface thiol identified on the IL-2 receptor may be a candidate for oxidation on cells from patients with chronic inflammatory diseases such as rheumatoid arthritis and thus contribute to the aberrant function of T cells in these patients.
Localization of tumour necrosis factor production in cells at the materno/fetal interface in human pregnancy
Authors: VINCE G , SHORTER S , STARKEY P , HUMPHREYS J , CLOVER L , WILKINS T , SARGENT I , REDMAN C 
Published: July 2010

SUMMARYBiologically active tumour necrosis factor (TNF) was detected in medium conditioned by incubation with cxplants of human pregnancy decidua or fetal chorionic villous tissue, taken in the first trimester and at term. Addition of endotoxin increased TNF release in most cases. ELISA assays gave similar results for TNF–α and also demonstrated low levels of TNF–β. Using cell populations purified by flow cytometry, secretion of biologically active TNF was shown to be localized to the macrophages. Cytotrophoblast purified from term amniochorion produced no TNF. Both decidual and chorionic villous tissue at term contained mRNA for TNF–α and TNF–β. TNF–α mRNA was confined to decidual macrophages in first trimester tissue, and was not present in chorionic cytolrophoblast. TNF–β mRNA, in contrast, was detected in both macrophage and no-acrophage populations in term dccidua.
Characterization of IL-1 inhibitory factor released from human alveolar macrophages as IL-1 receptor antagonist
Authors: TAKEUCHI M , NAGAI S , NAKADA H , AUNG H , SATAKE N , KANESHIMA H , IZUMI T 
Published: July 2010

SUMMARYIL-1 possesses pleiotropic properties on various cells and its activity may be stringently regulated in several ways. We have previously reported that both IL-1 and its inhibitory factor are concomitantly released from alveolar macrophages in both healthy subjects and patients with chronic inflammatory lung diseases. An increase in IL-1 activities and a decrease in inhibitory activities arc characteristics found in both healthy smokers and patients with interstitial lung diseases. In this study, we further examined the biological properties of IL-1 inhibitory factor. The inhibitor exhibited a dose-dependent specific inhibition of an augmentation by IL-1 of PH-nduced murinc thymocyte proliferation, while no inhibition of the augmentation by IL-2, IL-4, IL-6, or tumour necrosis factor (TNF) was found. 125I-labelled IL-1α binding on PHA-stimulated murinc thymocytes revealed two types of IL-1 binding sites. 44 sites/cell with a Kd of 2.7 ± 10−10 m and 230 sites/cell with a Kd of 2.5 ± 10−9 m. Alveolar macrophage culture supernatants blocked the binding of labelled IL-1 to the IL-1 receptor in a dos-ependent fashion. Scatchard plot analysis revealed that the inhibitory factor in the supernatants blocked the binding competitively. These results indicate that alveolar macrophages produce a specific IL-1 inhibitory factor, functioning as an IL-1 receptor antagonist.
During HIV-1 infection most blood dendritic cells are not productively infected and can induce allogeneic CD4+ T cells clonal expansion
Authors: CAMERON P U , FORSUM U , TEPPLER H , GRANELLI-PIPERNO A , STEINMAN R M 
Published: July 2010

SUMMARYWe have considered the possibility that antigen-presenting cells of the dendritic cell lineage may be infected in vivo and spread HIV-1 at the time dendritic cells initiate the clonal expansion of antigen-specific T cells. Dendritic cells were isolated from 25 HIV-1–infected subjects (CDC stages II- IV). Fewer dendritic cells were recovered from most infected subjects. Reduced numbers of total non-T cells were also found in these patients, so that preferential loss of dendritic cells did not occur. Dendritic cell function was assessed by stimulatory capacity for allogeneic CD4+ T cells in the mixed leucocyte reaction (MLR). Potent M LR stimulator activity was retained in the dendritic cell-enriched populations from HIV-infected patients. Seven out of nine patients without AIDS (asymptomatic, lymphadenopathy or ARC) and three out of six patients with AIDS had proliferative responses equivalent to those induced by dendritic cells from controls. Dendritic cells from HIV+ subjects were able to initiate the expansion of allogeneic CD4+ T cell clones with cloning efficiency not different from controls and without evidence of cytopathic effect in the expanding CD4+ clones. In situ hybridization of the different mononuclear cell populations with a gag-specific riboprobe demonstrated positive cells in the T cell fractions of 12 of the 15 patients tested. None of the asymptomatic or ARC patients had riboprobe-positive cells in the dendritic cell-enriched populations. Four out of nine patients with AIDS had cells positive for HIV-1 expression in the dendritic cell-enriched fraction. However, the positive cells had the nuclear profile of lymphocytes, and by cytofluorography some residual low-density T cells were present. By limiting dilution and polymerase chain reaction (PCR), CD4+ lymphocytes carried HIV provirus in inocula of 500–5000 cells, while provirus could only be detected in 50000 cells from the dendritic cell-enriched fraction. The latter signal may be due to the demonstrated levels of T cell contamination. Our data indicate that productive or latent HIV-1 infection of blood dendritic cells in vivo is rare, certainly no greater than in T lymphocytes, and that in vitro dendritic cell preparations from patients can expand CD4’ T cells efficiently and therefore may be able to expand T cells with immunotherapeutic activity.
Laboratory control values for CD4 and CD8 T lymphocytes. Implications for HIV-1 diagnosis
Authors: BOFILL M , JANOSSY G , LEE C A , MACDONALD-BURNS D , PHILLIPS A N , SABIN C , TIMMS A , JOHNSON M A , KERNOFF P B A 
Published: July 2010

SUMMARYWith the advent of standard flow cytometric methods using two-colour fluorescence on samples of whole blood, it is possible to establish the ranges of CD3. CD 4 and CDS T lymphocyte subsets in the routine laboratory, and also to assist the definition of HIV-1-related deviations from these normal values. In 676 HIV-1-seronegative individuals the lymphocyte subset percentages and absolute counts were determined. The samples taken mostly in the morning. The groups included heterosexual controls, people with various clotting disorders but without lymphocyte abnormalities as well as seronegative homosexual men as the appropriate controls for the HIV-1-infected groups. The stability of CD4% and CD8% values was demonstrated throughout life, and in children CD4 values &lt; 25% could be regarded as abnormal. The absolute counts of all T cell subsets decreased from birth until the age of 10 years. In adolescents and adults the absolute numbers (mean±s.d.) of lymphocytes, CD3, CD4 and CD8 cells were 1·90±0·55, 1·45±0·46, 0·83±0·29 and 0·56± 0·23 ± 109/l, respectively. In patients with haemophilia A and B the mean values did not differ significantly. In homosexual men higher CD8 levels were seen compared with heterosexual men and 27% had an inverted CD4/CD8 ratio but mostly without CD4 lymphopenia (CD4&lt;0·4 ± 109/l). However, some healthy uninfected people were‘physiologically’ lymphopenic without having inverted CD4/CD8 ratios. When the variations‘within persons’ were studied longitudinally over a 5-year period, the absolute CD4 counts tended to be fixed at different levels. As a marked contrast, over 60% of asymptomatic HIV-1+ patients exhibited low CD4 counts &lt;0·4 ± 109/l together with inverted CD4/CD8 ratios. Such combined changes among the heterosexual and HIV-1-seronegative homosexual groups were as rare as 1·4% and 3%, respectively. For this reason, when the lymphocyte tests show &lt;0·4 ± 109/l CD4 count and a CD4/CD8 ratio of less than unity, the individuals need to be investigated further for chronicity of this disorder, the signs of viral infections such as HIV-1 and other causes of immunodeficiency.
Tumour necrosis factor, IL-1 and IL-6 in bronchoalveolar washings and theirin vitroproduction duringNippostrongylus brasiliensisinfection
Authors: BENBERNOU N , MATSIOTA-BERNARD P , JOLIVET C , OUGEN P , GUENOUNOU M 
Published: July 2010

SUMMARYBronchoalveolar washings (BAW) were obtained from rats primarily infected with N. brasiliensis during the early infection stage that coincides with the lung passage of the parasite and the recruitment of inflammatory cells. BAW were tested for IL-1, IL-6 and tumour necrosis factor (TNF) activities. We found that IL-1 production occurred only on day 1 post infection and ceased thereafter. IL-6 activity was present as from day 1 with a maximum on day 3 post infection and then returned to its normal levels on day 5 post infection. TNF activity was not recovered in BAW at any time of the early infection. Results obtained from the in vitro culture of BAW-adhcrent cells demonstrated that on day I post infection IL-1, but also large amounts of TNF were produced spontaneously, whereas IL-6 was continuously released. Bacterial lipopolysaccharide (LPS) stimulation of the cell culture resulted in an amplification of the cytokine production. Our results suggest that pulmonary cytokincs detected in BAW were at least in part produced by alveolar macrophages. Furthermore, the kinetics of IL-1, TNF and IL-6 production show that these monokines are induced at different times during the course of infection, suggesting that cytokine production may follow different regulation patterns during the early phase of N. bransiliensis infection.
Apoptosis in human thymocytes after treatment with glucocorticoids
Authors: NIETO M A , GONZÁLEZ A , GAMBÓN F , DÍAZ-ESPADA F , LÓPEZ-RIVAS A 
Published: July 2010

SUMMARYTreatment of unfractionated human thymocytes in culture with the synthetic glucocorticoid dexamethasone induced cell death, as measured by trypan blue exclusion, after several hours of incubation. In purified subsets of human cortical and medullary thymocytes dexamethasone caused cell lysis with similar kinetics in both populations; 50% of thymocytes were killed after 20–24 h of incubation with the steroid. The mechanism of dexamethasone-induced cell death seems to correspond to apoptosis since degradation of DNA into oligonucleosome-sized fragments could be observed in the cultures treated with the steroid. A certain degree of DNA fragmentation and cell death could also be observed in control cultures of thymocytes. In contrast, peripheral T lymphocytes were resistant to the cytolytic effect of glucocorticoid hormone. The killing of human thymocytes by dexamethasone was inhibited by cycloheximide, suggesting that this cell death program requires a fully operating protein synthesis machinery and perhaps the induction of new proteins.
Relationship between a novel human cytotoxin (factor 2) produced by a B cell line (Karpas 160) and phorbol-myristateacetate-associated cytotoxicity
Authors: NI J , KARPAS A 
Published: July 2010

SUMMARYWe found that 160b cells, a subclone of Karpas 160 human B cell line, spontaneously secreted a novel cytotoxin, factor 2 (F2). F2 was also extracted from the cells by 60% ammonium sulphate. 0·5% CHAPS and 0·28% Triton X-114. We were able to show that phorbol myristate acetate (PMA) greatly enhanced the production of F2, and PMA may also account for part of the putative F2 cytotoxic activity to K562 cells in crude preparations. We compared the cytotoxic effect of F2 with PMA-associated F2-like cytotoxicity to K562 cells as well as the adequacy of our schemes to purified F2 with regard to its separation from PMA. We found that it was possible to separate PMA from F2 preparations by gel filtration and Rotofor preparative isoelectric focusing. The fate of PMA was also monitored with 3H-PMA and chromatographic profiles of 3H-PMA were studied using DE52 and gel filtration chromatography. We were able to establish that less than 2·9% of the cytotoxicity to K562 was due to PMA. We also found that the radioactive peaks and cytotoxicity peaks to K562 were not well correlated, indicating that the cytotoxicity was not mainly due to remaining PMA. Activated charcoal removed virtually all F2 and PMA but not tumour necrosis factor activity. Our results also showed that cytotoxicity to K562 resulting from F2 or PMA-associated proteins had different physicochemical properties, indicating that they are different molecular entities. These findings are consistent with the earlier observation that 160 cells produce F2 spontaneously and that PMA can amplify its production significantly.
Characterization of the lymphocytic alveolitis in visna-maedi virus-induced interstitial lung disease of sheep
Authors: CORDIER G , GUIGUEN F , CADORÉ J L , COZON G , JACQUIER M F , MORNEX J F 
Published: July 2010

SUMMARYIn order to investigate the contribution of lymphocytes to interstitial lung disease in animals with visna-maedi infection, we studied in parallel bronchoalveolar cells and lung tissue from slaughterhouse animals (n = 29) and from colostrum-deprived lambs transtracheally inoculated with field isolates of visna-maedi virus (n = 9) or saline (n = 6). Lymphocyte subpopulations were identified in bronchoalveolar lavagc by immunofluorescence and flow cylomctry analysis and in lung tissue using indirect immunohistochemistry. In infected animals a lymphocytic alveolitis containing CD4 and CD8 lymphocytes was observed. Pcribronchovascular lymphoid nodules comprise mostly CD4 lymphocytes. Alveolar lymphocytes of both subsets displayed increased expression of MHC class II antigens in animals with naturally occurring maedi but not in experimentally infected ones. A sequential process of lymphocyte attraction and activation is likely to occur in vivo as part of the alveolitis.
Alterations in mononuclear cell tumour necrosis factor-alpha (TNF-a) response in patients on long term cuprophane haemodialysis
Authors: ANNENKOV A Y , STROKOV A G , BARANOVA F S 
Published: July 2010

SUMMARYWe have investigated TNF-a secretory response of peripheral blood mononuclear cells (PBMC) from 13 uraemic patients undergoing regular haemodialysis with cuprophane membrane (CM). Sixteen healthy subjects and five uraemic patients under conservative therapy were also studied as controls. Cells of haemodialysis patients exhibited increased TNF-a release in vitro in the absence of activating stimuli other than culture conditions, as compared with normal and uraemic controls. In contrast to normal cells, this spontaneous secretion of TNF-a from dialysis PBMC could not be significantly reduced by addition of polymyxin B to culture medium, thus indicating its independence of trace amount of lipopolysaccharide (LPS) present in the medium as contaminant. Furthermore, prc-dialysis PBMC were considerably more sensitive to stimulation with It)7 pg/ml of LPS under in vitro culture conditions than normal and uraemic controls. To elucidate a role of direct contact with CM in stimulation of TNF-a release from monocytes. PBMC were cultured on CM in vitro. Contact with CM stimulated TNF-a secretion from PBMC above the level of cells cultured on tissue culture plastic. This response persisted with time in culture in contrast to a transient LPS-induccd TNF-a release. Furthermore. PBMC stimulated by contact with CM for 2 days did not lose the capacity to secrete TNF-a in response to a subsequent LPS stimululion, while a 2-day treatment of cells with LPS was followed by LPS refractory slate. Therefore, direct contact with CM induces in PBMC a long-lasting TNF-a response which is not down-regulated by the acquisition of refractoriness in a manner similar to that which occurs in the case of LPS stimulation. These in vitro findings provide a possible explanation of the observation that predialysis PBMC exhibit elevated TNF-a secretory capacity.
The role of O-antigen polysaccharide in the activation of neutrophils by lipopolysaccharides ofSalmonellaspecies
Authors: RASOOL O , NNALUE N A , JARSTRAND C 
Published: July 2010

SUMMARYActivation of neutrophils by lipid A, O-antigen polysaccharides (PS) and smooth lipopolysacchar ides (LPS) isolated from Salmonella choleraesuis (O-6,7) and Salmonella typhimurium (O-4,5,12) was investigated. The methods used were assays for lysozyme release and for nitroblue tetrazolium (NBT) reduction which measures the level of oxidative metabolism of neutrophils. LPS from both species stimulated neutrophils to the same extent in the presence of autologous plasma. In the absence of plasma only the O-6,7 LPS activated neutrophils. Lipid A of PS isolated from both LPS either did not activate neutrophils of did so only at very high concentrations when tested in the presence of plasma; in the absence of plasma no activation occurred. The data indicate that both PS and lipid A segments of LPS are required for activation of neutrophils by LPS. We also deduce that plasma, probably complement, is required for the interaction of some LPS, e.g. 0–4,5,12 with neutrophils whereas other LPS, e.g. 0–6,7 can interact directly and activate neutrophils.
Endothelial cell damage in primary biliary cirrhosis: influence of cholestasis and immunological mechanisms
Authors: BLANN A D , BABBS C , NEUBERGER J M 
Published: July 2010

SUMMARY
In a study looking for evidence of endothelial cell damage in primary biliary cirrhosis, serum from patients was found to be significantly more cytotoxic to cultured endothelial cells in vitro than normal control serum (P&lt;0·001). Serum also contained higher levels of von Willebrand factor antigen (vWFAg, a specific product of the endothelium) than control serum (P&lt;0·001). Cytotoxicity correlated with serum levels of vWFAg (P&lt;0·05) and with serum bilirubin (P&lt;0·05). No correlations were found between cytotoxicity and circulating immune complexes. C-reaetive protein or CH50. The study was controlled by serum from patients with other liver diseases. In these samples vWFAg (P&lt;0·003), and bilirubin levels (P&lt;0·001) were also raised relative to normal controls. vWFAg levels again correlated with levels of bilirubin (P&lt;0·05). Tissue culture experiments showed that purified bilirubin was cytotoxic to human umbilical vein endothelial cells and induced the release of vWFAg. The case report of a patient with obstructive jaundice again indicated that levels of bilirubin and vWFAg were related. These results suggest that endothelial cell damage occurs in both primary biliary cirrhosis and to a lesser extent in other liver diseases, and may be mediated by cholestasis, not by humoral immunological mechanisms.