bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differentiation antigens on rhesus monkey lymphocytes I. Identification of T cells bearing CD3 and CD8, and of a subset of CD8‐bearing cells
Authors: Nooij Frans J. M. , Borst Jannie G. , Van Meurs Gerard J. E. , Jonker Margreet , Balner Hans 
Published: February 2007

AbstractRhesus monkeys provide an excellent preclinical model to test the effect of monoclonal antibodies (mAb) in vitro and in vivo. So far, mostly mAb have been used which were originally raised against human cell surface antigens but cross‐reacted reasonably well with homologous antigens on rhesus monkey cells. However, to optimize the model, it was necessary to produce mAb which react specifically with subsets of rhesus monkey lymphocytes. In this report, three mouse anti‐rhesus monkey mAb are described, specific for different subsets of rhesus monkey T lymphocytes. None of the reagents cross‐reacts with human lymphocytes. Characterization of these mAb was based upon indirect immunofluorescence, using a simultaneous staining technique, and immunoprecipitation of the specific target antigens. One antibody (GM9) reacts with the same subset as is recognized by mAb specific for human CD8+cells. The second mAb (GM13) is specific for a subset of CD8+ cells. A third mAb (FN18) was of particular interest: it identifies a cell surface complex, RhT3, expressed on mature T lymphocytes, of which the polypeptide chains have a molecular mass of 22 and 27 kDa. The data strongly suggest that RhT3 is a CD3‐like determinant, so far unidentified in the rhesus monkey.
Heterogeneity of responsiveness of chronic lymphocytic leukemic B cells to B cell growth factor or interleukin 2
Authors: Hivroz Claire , Grillot‐Courvalin Catherine , Brouet Jean‐Claude , Seligmann Maxime 
Published: February 2007

AbstractWe compared the proliferative responses of purified human leukemic B cells from 12 cases of chronic lymphocytic leukemia to highly purified B cell growth factor (BCGF) and recombinant interleukin 2 (rIL 2) spontaneously, and in a coactivation assay using anti‐μ monoclonal antibodies. Heterogeneity of response to one or the other lymphokine was observed from case to case. Spontaneous responses were observed to BCGF in one case, to rIL 2 in 3 cases and to both lymphokines in one other case. Costimulation with anti‐μ monoclonal antibody induced a proliferative response to BCGF in 3 additional cases and to rIL 2 in 4 cases. Interestingly, cells from BCGF‐ responsive cases also proliferated in response to rIL 2. The leukemic B cells from 4 chronic lymphocytic leukemia patients were unresponsive. Cells from 5 cases expressed IL 2 receptors, although rIL 2 induced a direct proliferative response in only 3 of these cases. Expression of the B cell activation antigen B5 was associated to BCGF responsiveness.
Presence of IgE suppressor factors in human colostrum
Authors: Sarfati Marie , Vanderbeeken Yves , Rubio‐Trujillo Manuel , Duncan Doug , Delespesse Guy 
Published: February 2007

AbstractIn spite of intensive investigations, the ability of breast feeding to delay and to attenuate atopic diseases in children remains debatable. This study documents a mechanism whereby breast feeding might interfere with the synthesis of IgE by breast‐fed infants. Indeed, we show that colostrum contains IgE‐binding factors (IgE‐BF) capable of suppressing the in vitro synthesis of human IgE. Colostrum obtained from 15 donors was successively depleted of lipids and casein, filtered through Amicon XM50 membrane (mol. mass cut‐off 50 kDa) and lyophilized. IgE‐BF was demonstrated in such preparations by two different approaches, i.e. a classical rosette inhibition assay and Western blot analysis. In the first instance, lyophilized preparations of colostrum inhibited the binding of IgE‐coated bovine erythrocytes to IgE receptors on the surface of RPMI 8866 lymphoblastoid cells. The rosette‐inhibiting activity could be absorbed on IgE‐ but not on IgG‐Sepharose 4B and it could be recovered in the eluate of IgE‐Sepharose 4B. The molecular mass of IgE‐BF was comprised between 10 to 20 kDa as estimated by gel filtration through a calibrated Sephadex G‐75 column. After fractionation on 12% sodium dodecyl sulfate‐polyacrylamide gel electrophoresis and transfer to nitrocellulose membrane, colostrum displayed one band of 14 kDa and reacted with radiolabeled IgE but not with IgG nor IgM. This 14‐kDa band could be removed by absorbing colostrum with IgE‐ but not with IgG‐Sepharose 4B. Most importantly, the colostrum IgE‐BF suppressed the spontaneous in vitro synthesis of IgE by B lymphocytes derived from allergic donors without altering the production of IgM.
Administration of recombinant interleukin 2 to mice enhances production of hemopoietic and natural killer cells
Authors: Piguet Pierre‐Fragois , Grau Georges , Irle Claude , Vassalli' P. 
Published: February 2007

AbstractSeven days of continuous perfusion of mice with human recombinant interleukin 2 (rIL 2) (∼ 3 × 104 U/day) increased the percentage of large mononuclear leukocytes (LML) among bone marrow, spleen, lymph node cells and liver interstitial cells (LIC). An increase in the lymphokine‐activated killer (LAK) activity was evident in these organs. The greatest increase in the number of LML and in the LAK activity was observed among the liver interstitial cells (about 500‐fold increase). The LML were nonphagocytic, Thy‐l+, sIg−, Ly 2+, L3T4− and asialo Gm1+. Perfusion of athymic nude mice, or of thymectomized, irradiated radiation chimera, showed that the Thy‐l+, LAK+ LML were the thymus and T lymphocyte‐independent progeny of Thy‐1−marrow precursors. The LML had no T cell function in a graft‐ vs. ‐host reactivity assay, neither did they have an inhibitory effect on T lymphocyte function in vivo. rIL 2 perfusion did not significantly affect the medullary hemopoiesis but did strongly enhance the extramedullary hemopoiesis, particularly within the interstice of the liver: the number of erythroid and myeloid cell was increased as well as the number of colony‐forming units per spleen and colony‐forming units per culture for various lineages (20‐50‐fold increment). These results show that in vivo, rIL 2 has a global enhancing effect on hemopoiesis together with a more selective influence on the production of LML.
Accessory molecules and T cell activation I. Antigen receptor avidity differentially influences T cell sensitivity to inhibition by monoclonal antibodies to LFA‐1 and L3T4
Authors: Regnier‐Vigouroux Anne , Blanc Dominique , Pont Suzanne , Marchetto Sylvie , Pierres Michel 
Published: February 2007

AbstractA series of BALB/c‐derived T hybridoma cells, capable of producing interleukin 2 (IL2) in response to poly(Glu60, Ala30, Tyr10) (GAT) presented by syngeneic B lymphoma cells in the context of Ad restriction determinants, was used as a model system to evaluate the roles of LFA‐1 and L3T4 accessory molecules in antigen‐specific T cell activation. Examination of the antigen requirement for optimal IL2 responses revealed marked differences in the apparent avidity of these cells for GAT/Ad complexes. A relationship was observed between this parameter and the susceptibility of T hybridoma cells to inhibition by monoclonal antibodies directed at 5 distinct epitopes of LFA‐1, and at Aβd allodeterminants. In contrast, L3T4a‐specific monoclonal antibodies were found to block in a similar fashion the antigen‐specific IL2 responses of T hybridoma cells, regardless of the apparent avidity of their antigen receptors. It was also shown that both L3T4+ and L3T4− T hybridoma cells were capable of recognizing GAT plus Ad with high avidity. Thus, the quality of T cell antigen recognition appears to critically influence the involvement of LFA‐1, and only to a marginal extent that of L3T4, in antigen‐specific T cell activation. The implications of these findings are discussed in the context of recent data indicating that L3T4 may not only be an la‐binding protein.
An attempt to produce “pre‐T” cell hybridomas and to identify their antigens
Authors: Aihara Yukoh , Bühring Hans‐Jörg , Aihara Michiko , Klein Jan 
Published: February 2007

AbstractWith the aim of identifying some of the stages in the development of pre‐T cells (cells of the T cell lineage before they enter the thymus), we have produced a large number of hybridomas by the fusion of BALB/c bone marrow cells, bone marrow cells from BALB/c‐nu/nu mice, BALB/c fetal liver cells and BALB/c fetal thymocytes with the AKR thymoma BW5147. The hybridomas were selected for the expression of the Thy‐1.2 antigen of th3 normal celldonor and for their ability t9produce interleukin 2 (IL 2) upon co‐culture with irradiated normal spleen cells. A set of these hybridomas is described in this communication. The hybridomas were then used to immunize rats and to generate monoclonal antibody‐producing B cell hybridomas. Most, if not all, of the immunizing hybridomas were derived from pre‐T cells as evidenced by the fact that they produce IL 2, and express some of the T cell markers (the Thy‐1.2, Ly‐1, Ly‐2 or L3T4 antigens). The monoclonal antibodies were tested on a panel of pre‐T cell hybridomas and on normal cells obtained from spleen, lymph nodes, thymus and bone marrow. The testing was carried out by the microcytotoxicity assay and flow cytometric analysis. Three groups of antibodies could be distinguished. Some antibodies were broadly reactive, being positive with virtually all the clones in the pre‐T cell panel and with a substantial fraction of normal lymphoid cells. The identity of the antigens detected by these antibodies remains unknown but they do not seem to correspond to any of the known cell surface markers. Other antibodies reacted only with some of the pre‐T cell clones and did not react at all with normal lymphoid cells obtained from adult animals. Finally, other antibodies still reacted only with a minor subpopulation of thymocytes or of thymocytes and bone marrow cells, as well as some of the pre‐T cell clones; they did not react with spleen and lymph node cells. These antibodies might be specific for cells in the prethymic phase of the T cell differentiation pathway. They should prove useful for the identification of pre‐T cell markers and hence for the isolation of pre‐T cells and their functional analysis.
Modulation of surface T11 molecules induced by monoclonal antibodies: analysis of the functional relationship between antigen‐dependent and antigen‐independent pathways of human T cell activation
Authors: Moretta Alessandro , Olive Daniel , Poggi Alessandro , Pantaleo Giuseppe , Mawas Claude , Moretta Lorenzo 
Published: February 2007

AbstractPrevious data indicated that T lymphocyte activation can be achieved by using a combination of anti‐T11 monoclonal antibodies (mAb) directed to the “T112” and the “T113” epitopes, respectively. Unlike the T cell activation induced by antibodies directed to the T3‐T cell receptor (Ti) complex or to T44 molecules, the anti‐T11 mAb‐induced cell activation was not accompanied by surface modulation of the T11 antigen. In the present study we show that appropriate stimulatory combinations of anti‐T11 mAb are able to induce T11 antigen modulation in a variety of T cells including polyclonal peripheral blood populations, normal as well as leukemic (JA3) T cell clones. The first anti‐T11 mAb combination leading to both cell activation and T11 antigen modulation was given by a mAb directed to the T112 epitope and by another mAb recognizing an epitope belonging to the T111 group. The second combination was given by two mAb directed against two different determinants of the T111group. The ability to induce T11 antigen modulation allowed a more precise analysis of the pathway of T cell activation initiated by T11 molecules and its physical and functional relationship with the other known pathways of T cell activation. T cells following T11 antigen modulation failed to respond to subsequent stimulation with anti‐T11 mAb. The refractory period lasted for 48–72 h and the restoration of the responsiveness to anti‐T11 mAb coincided with the re‐expression of T11 molecules at the cell surface. Modulation of T11 antigen did not affect the surface expression of T3, Ti or T44 molecules, in addition, “modulated” cells maintained their ability to respond to mAb directed against T3, Ti or T44 molecules. On the contrary, antibody‐induced modulation of the T3‐Ti receptor complex abrogated both T11‐ and T44‐dependent T cell activation. Finally, antibody‐induced modulation of T44 antigen did not inhibit either the T11‐ or the T3‐Ti‐dependent pathway of T cell activation. These data indicate that down‐regulation of the pathway of T cell activation initiated by T11 molecules can be induced not only by modulation of the antigen receptor complex but also by appropriate mAb to T11 molecules and, presumably, by the natural ligand binding to T11 molecules.
Identity between human interferon‐γ and “macrophage‐activating factor” produced by human T lymphocytes
Authors: Talmadge Kenneth W. , Gallati Harald , Sinigaglia Francesco , Walz Alfred , Garotta Gianni 
Published: February 2007

AbstractHuman peripheral blood monocytes purified by counterflow elutriation were activated in vitro by human natural or recombinant interferon‐γ (IFN‐γ) as shown by enhanced killing of Listeria monocytogenes and increased production of H2O2 in response to phorbol myristate acetate. Half‐maximal stimulation for macrophage activation (MAF) was observed with 10–20 antiviral U/ml of purified recombinant IFN‐γ. These MAF activities were found to correlate with the antiviral activity dependent on IFN‐γ under several experimental conditions. Both activities were recovered together from supernatants of concanavalin A‐stimulated peripheral blood mononuclear cells and in the media of a large number of T cell clones of different specificities. The parallelism between the two activities was also observed upon fractionation of culture media from producing cells and upon treatment of such preparations with low pH and high temperature. Finally, three antibodies with different specificities were found to abrogate the MAF and antiviral activities from lymphocyte culture supernatant. These results indicate that MAF released by stimulated lymphocytes is identical to IFN‐γ.
Function of the LFA‐1 and T4 molecules in the direct activation of resting human B lymphocytes by T lymphocytes
Authors: Tedder Thomas F. , Schmidt Reinhold E. , Rudd Christopher E. , Kornacki Mary M. , Ritz Jerome , Schlossman Stuart F. 
Published: February 2007

AbstractActivated T lymphocytes can provide all of the signals necessary to induce the proliferation of resting B lymphocytes. The activation signal is presumably initiated through direct T‐B lymphocyte contact. The role of the leukocyte function antigen‐1 (LFA‐1) and T4 molecules in the activation of purified, small B lymphocytes by mitomycin C‐treated T lymphocytes was examined by using monoclonal antibodies that react with and inhibit the function of these molecules. Anti‐LFA‐1 antibody binding significantly inhibited T‐B lymphocyte interactions that result in B lymphocyte proliferation. In contrast, the presence of anti‐T4 antibodies at concentrations as high as 100 μg/ml did not inhibit this interaction. These results indicate that the B lymphocyte activation signal may not be mediated through the interaction of T4 molecules with major histocompatibility complex class II antigens of the B lymphocyte but is a cell‐cell contact‐dependent event that is facilitated by LFA‐1 molecules.
Tumor‐promoting phorbol esters suppress receptor‐stimulated inositol phospholipid degradation and Ca2+ mobilization in mouse lymphocytes
Authors: Bijsterbosch Martin K. , Klaus Gerry G. B. 
Published: February 2007

AbstractAnti‐immunoglobulin antibodies (anti‐Ig) provoke the rapid breakdown of phos‐phatidylinositol bisphosphate (PIP2), elevation of cytoplasmic Ca2+ levels ([Ca2+]i) and activation of protein kinase C (PKC) in B lymphocytes. Tumor‐promoting phorbol esters, like phorbol myristate acetate, also activate PKC, but inhibit anti‐Ig‐induced B cell proliferation. To investigate the basis of the latter effect, we studied the influence of phorbol esters on PIP2 degradation and [Ca2+]i in murine B cells. The results show that PKC‐activating phorbol esters cause marked inhibition of anti‐Ig‐stimulated PIP2 breakdown and Ca2+ mobilization. In addition, these agents inhibit concanavalin A‐provoked Ca2+ influx, lower resting cytoplasmic Ca2+ levels and reduce ionophore‐induced Ca2+ influx in B cells. Apparently, PKC stimulation causes feedback inhibition of receptor signalling, not only by suppressing PIP2 degradation, but also by exerting additional complex effects on the control of [Ca2+]i in B cells. It is, however, not clear how these findings relate to the anti‐proliferative effects of phorbol esters on B cells.
Micro‐ and Nano‐ Magnetic Particles for Applications in Biosensing
Authors: Hsing I‐Ming , Xu Ying , Zhao Wenting 
Published: February 2007

AbstractThis article reviews the development of electrochemical biosensors, incorporating magnetic particles, for detecting biomolecules (nucleic acids and proteins) and cells. Magnetic particles (MPs) of micro‐ and nanoscale, mimicking the size of molecules in nature, possess interesting characteristics that facilitate the purification and detection of biomolecules in a wide range of samples. In particular, the high surface area and the paramagnetic or superparamagnetic properties of these tiny particles provide an attractive technology platform for the design of electrochemical biosensors. Examples of electrochemistry‐based approaches to achieve the separation and detection of bioentities utilizing MPs are described. Emphasis is placed on the strategies to incorporate the electrochemical labels to the MPs and the methods to achieve the dual function of electrochemical detection and magnetic separation. The protocols to make MPs as labels in biological sensors are also discussed.
Full‐scale experimental verification of resetable semi‐active stiffness dampers
Authors: Yang J. N. , Bobrow J. , Jabbari F. , Leavitt J. , Cheng C. P. , Lin P. Y. 
Published: February 2007

AbstractBecause of many advantages over other control systems, semi‐active control devices have received considerable attention for applications to civil infrastructures. A variety of different semi‐active control devices have been studied for applications to buildings and bridges subject to strong winds and earthquakes. Recently, a new semi‐active control device, referred to as the resetable semi‐active stiffness damper (RSASD), has been proposed and studied at the University of California, Irvine (UCI). It has been demonstrated by simulation results that such a RSASD is quite effective in protecting civil engineering structures against earthquakes, including detrimental near‐field earthquakes. In this paper, full‐scale hardware for RSASD is designed and manufactured using pressurized gas. Experimental tests on full‐scale RSASDs have been conducted to verify the hysteretic behaviours (energy dissipation characteristics) and the relation between the damper stiffness and the gas pressure. The correlation between the experimental results of the hysteresis loops of RASADs and that of the theoretical ones has been assessed qualitatively. Experimental results further show the linear relation between the gas pressure and the stiffness of the RSASD as theoretically predicted. Finally, shake table tests have also been conducted using an almost full‐scale 3‐storey steel frame model equipped with full‐scale RSASDs at the National Center for Research on Earthquake Engineering (NCREE), Taipei, Taiwan, and the results are presented. Experimental results demonstrate the performance of RSASDs in reducing the responses of the large‐scale building model subject to several near‐field earthquakes. Copyright © 2007 John Wiley & Sons, Ltd.
Expected value of sample information for Weibull survival data
Authors: Brennan Alan , Kharroubi Samer A. 
Published: February 2007

AbstractExpected value of sample information (EVSI) involves simulating data collection, Bayesian updating, and re‐examining decisions. Bayesian updating in Weibull models typically requires Markov chain Monte Carlo (MCMC).We examine five methods for calculating posterior expected net benefits: two heuristic methods (data lumping and pseudo‐normal); two Bayesian approximation methods (Tierney & Kadane, Brennan & Kharroubi); and the gold standard MCMC. A case study computes EVSI for 25 study options. We compare accuracy, computation time and trade‐offs of EVSI versus study costs.Brennan & Kharroubi (B&K) approximates expected net benefits to within ±1% of MCMC. Other methods, data lumping (+54%), pseudo‐normal (−5%) and Tierney & Kadane (+11%) are less accurate. B&K also produces the most accurate EVSI approximation. Pseudo‐normal is also reasonably accurate, whilst Tierney & Kadane consistently underestimates and data lumping exhibits large variance. B&K computation is 12 times faster than the MCMC method in our case study. Though not always faster, B&K provides most computational efficiency when net benefits require appreciable computation time and when many MCMC samples are needed.The methods enable EVSI computation for economic models with Weibull survival parameters. The approach can generalize to complex multi‐state models and to survival analyses using other smooth parametric distributions. Copyright © 2007 John Wiley & Sons, Ltd.
Lebectin, a Macrovipera lebetina venom‐derived C‐type lectin, inhibits angiogenesis both in vitro and in vivo
Authors: Pilorget Anthony , Conesa Magali , Sarray Sameh , Michaud‐Levesque Jonathan , Daoud Salma , Kim Kwang Sik , Demeule Michel , Marvaldi Jacques , El Ayeb Mohamed , Marrakchi Naziha , Béliveau Richard , Luis José 
Published: February 2007

AbstractIntegrins play an essential role in endothelial cell motility processes during angiogenesis and thus present interesting targets for the development of new anti‐angiogenic agents. Snake venoms naturally contain a variety of proteins that can affect integrin–ligand interactions. Recently, the C‐type lectin proteins (CLPs) have been characterized as efficient modulators of integrin functions. In this study, we investigated the anti‐angiogenic activity of lebectin, a newly discovered CLP from Macrovipera lebetina venom. Human brain microvascular endothelial cells (HBMEC), used as an in vitro model, express αvβ3, αvβ5, and α5β1 integrins, as well as the α2, α3, α6, and β4 subunits. Our data show that lebectin acts as a very potent inhibitor (IC50 ≈ 0.5 nM) of HBMEC adhesion and migration on fibronectin by blocking the adhesive functions of both the α5β1 and αV integrins. In addition, lebectin strongly inhibits both HBMEC in vitro tubulogenesis on Matrigel™ (IC50 = 0.4 nM) and proliferation. Finally, using both a chicken CAM assay and a Matrigel™ Plug assay in nude mice, our results show that lebectin displays potent anti‐angiogenic activity in vivo. Lebectin thus represents a new C‐type lectin with anti‐angiogenic properties with great potential for the treatment of angiogenesis‐related diseases. J. Cell. Physiol. 211: 307–315, 2007. © 2007 Wiley‐Liss, Inc.