bluuebunny/crossref_metadata_2025_split huggingface dataset:
cDNA clones encoding immunoglobulin λ chains from rabbit expressing the phenotype c7
Authors: Hayzer David J. , Young‐Cooper Glendowlyn O. , Mage Rose G. , Jaton Jean‐Claude 
Published: March 2007

AbstractA cDNA library derived from spleen cells of an unimmunized rabbit expressing the c7 phenotype of Igλ chains (c7+, c21−) was screened with Vλ or Cλ probes of a λ light chain bearing c21 epitopes. The nucleotide sequences of three hybridizing clones were found to be identical within the Vλ, Jλ and Cλ regions. The Vλ region was 97% similar to that of the functional germ‐line gene Vλ2, and the Cλ region was identical to that of gene Cλ6, recently identified. Gene Cλ6 exhibited four codon differences when compared with gene Cλ5, the latter encoding c21 epitopes. The data presented here and in the accompanying report (Jaton, J.‐C. et al., Eur. J. Immunol. 1990. 20: 2713) support the view that gene Cλ6 encodes the C region of c7 λ chains and that c7 and c21 markers designate two distinct isotypic forms of λ chains. On the basis of comparative Southern blotting analyses and restriction maps of cloned genomic regions containing Vλ and Cλ genes, a scheme is proposed to account for the c7− and c21− phenotypes.
Isolation and characterization of IgG2a‐reactive autoantibodies from influenza virus‐infected BALB/c mice
Authors: Fazekas György , Rajnavölgyi ÉVa , Kurucz István , Sintár ÉVa , Kiss Katalin , László Glória , Gergely János 
Published: March 2007

AbstractRepeated influenza virus infection induces the production of dominantly IgG2a‐type virus‐specific antibodies as well as the appearance of IgG2a‐reactive autoantibodies in BALB/c mice characterized by low spontaneous rheumatoid factor‐type autoantibody production. IgG2a‐reactive autoantibody‐producing hybridomas could be isolated from the spleen of influenza virus‐infected BALB/c mice. The mAb produced by these clones represent not only IgM but also IgG and IgA isotypes and show strong isotype or isoallotype specificity. The common functional property of these autoantibodies is their preferential‐ and high‐affinity binding to complexed, solid‐phase‐bound or heat‐aggregated IgG2a when compared to native soluble or cell‐bound IgG2a‐The mechanism of induction and the possible biological function of these autoantibodies are discussed in the light of their fine specificity and functional properties.
Alpha heavy chain disease of patient MAL: structure of the non‐functional rearranged α gene translocated on chromosome 9
Authors: Pellet Pascale , Tsapis Andreas , Brouet Jean‐Claude 
Published: March 2007

AbstractAlpha heavy chain diseases (HCD) are lymphoproliferative disorders characterized by the production of truncated α immunoglobulin heavy chain without associated light chains, α HCD MAL is featured by multiple structural alterations of the α1 productive gene and on original t(9;14)(p11;q32) translocation involving the other rearranged α allele. We present here the structure of the der(9) chromosome. Sequence analysis provides evidence that the translocation occurred after local pairing of the two chromosomes mediated by an almost perfect nonameric sequence, followed by a staggered double‐strand break of chromosome 14. This translocation occurred on a V(D)J rearranged locus; unexpectedly, there were a deletion of the 3' part of the VH gene, several insertions of non‐immunoglobulin‐related genes and multiple mutations, i.e. alterations reminiscent of those occurring on the HCD productive genes.
The induction of skin graft tolerance in major histocompatibility complex‐mismatched or primed recipients: primed T cells can be tolerized in the periphery with anti‐CD4 and anti‐CD8 antibodies
Authors: Cobbold Stephen P. , Martin Gilly , Waldmann Herman 
Published: March 2007

AbstractMice given short courses of anti‐CD4 and anti‐CD8 monoclonal antibodies became tolerant of allogeneic skin grafted at the same time. Tolerance could be obtained without Tcell depletion across multiple minor antigen mismatches, both in naive and primed animals, demonstrating that peripheral T cells could be tolerized, even if they had been previously activated. Where donor and recipient were incompatible across the whole major histocompatibility complex, specific tolerance could be achieved by using a combination of depleting followed by non‐depleting antibodies, where each alone was unsuccessful. Although mice clearly tolerated their original skin grafts, we observed in some strain combinations that a second fresh, but genotypically identical graft, was slowly rejected. Such mice also possessed Tcells which could proliferate to donor‐type stimulator cells in vitro. Whatever the mechanisms, we have demonstrated that operational transplantation tolerance can be achieved with simple, non‐toxic antibody therapy. The introduction of comparable tolerance‐inducing regimens in clinical organ transplantation could obviate the need for long‐term immunosuppression and its unfortunate side effects.
A novel thymic epithelial adhesion molecule
Authors: Couture Clément , Patel Pravin C. , Potworowski Edouard F. 
Published: March 2007

AbstractInteractions between thymocytes and thymic stromal cells are responsible for positive and negative selection of T cells, their differentiation, maturation and proliferation. The signals required for these events to occur often necessitate close contact, and indeed adhesion, between the cell types involved. The identification of specific adhesion molecules in this context is, therefore, a vital first step in determining the nature of the signal they mediate or facilitate at a given stage of differentiation. In the present work we identify, isolate and partially characterize a ligand present on thymic medullary epithelial cells which selectively binds CD4+CD8+ thymocytes found primarily in the thymic cortex. This adhesion molecule is composed of two non‐covalently associated glycoproteins of 23 kDa and 45 kDa, respectively, both of which are needed to bind to thymocytes. The importance of the finding is that the ligand, in isolated immobilized form, binds the same thymocyte subset as the original epithelial cell line from which it was isolated. The CD4+CD8+ thymocyte subset is the precursor of single‐positive mature Tcells; hence the putative biological activity of the ligand in question takes place at a pivotal stage of Tcell differentiation.
A three‐dimensional model system to study the interactions between human leukocytes and endothelial cells
Authors: Hakkert Betty C. , Rentenaar Jeannette M. , Van Aken Willem G. , Roos Dirk , Van Mourik Jan A. 
Published: March 2007

AbstractLeukocyte adhesion to endothelial cells and migration into the subendothelial matrix was studied with a three‐dimensional model system, consisting of human endothelial cells cultured on a loose collagen matrix. We developed a new method to separate the endothelial cell monolayer and adhering leukocytes from the subendothelial matrix, allowing simultaneous analysis of leukocyte adhesion and transendothelial migration. Monocytes adhered more avidly to untreated endothelial cells than did neutrophils (2.5 ± 0.3 vs. 1.0 ± 0.2 leukocytes per endothelial cell). Only a small fraction (10%–20%) of these leukocytes migrated into the subendothelium. Pretreatment of endothelial cells with interleukin 1 (IL1) enhanced adhesion (20%), but not migration of monocytes. In contrast, neutrophil adhesion was markedly and in a time‐dependent manner increased by IL1 treatment (i.e. 200% after 6h and 110% after 24 h of IL1 treatment). Moreover, IL1 pretreatment enhanced neutrophil migration twofold. Activation of leukocytes with formyl‐methionyl‐leucyl‐phenylalanine (fMLP) enhanced both monocyte and neutrophil adhesion, but did not affect leukocyte migration. Under all conditions, monocyte adhesion was only partly (30%–40%) inhibited by monoclonal antibodies (mAb) against the common β subunit of the leukocyte‐cell adhesion molecules (LeuCAM; CD 18) and 25%–30% by mAb against the α subunit of LFA‐1 (CD11a). In contrast, mAb against the α subunits of Mac‐1 (CD11b) and p150, 95 (CD11c) were hardly effective. fMLP‐mediated neutrophil adhesion was reduced to below baseline levels by anti‐LeuCAM (CD18) mAb, whereas the LeuCAM contribution in IL 1‐mediated neutrophil adhesion was less pronounced and varied in time. IL 1‐mediated neutrophil migration, however, was completely blocked by anti‐LeuCAM mAb. fMLP‐mediated neutrophil adhesion was inhibited by mAb against the α subunits of Mac, while mAb against the α subunits of LFA‐1 and Mac‐1 both reduced IL 1‐mediated adherence. In summary, we describe a novel leukocyte adhesion/migration method and demonstrate that the contribution of the LeuCAM complex in leukocyte‐endothelium interaction varies depending on cell type and stimulus used.
Identification of two distinct phosphoproteins as components of the human B cell antigen receptor complex
Authors: Van Noesel Carel J. M. , Borst Jannie , De Vries Evert F. R. , Van Lier René A. W. 
Published: March 2007

AbstractIn human B cells, the molecules that, upon receptor occupancy, couple membrane immunoglobulin to intracellular signal transduction pathways have never been identified. We here describe two phosphoproteins as integral parts of the B cell antigen receptor complex. Membrane IgM is non‐covalently associated with a disulfide‐linked heterodimer of glycoproteins. These molecules can be demonstrated on B cell lines and freshly isolated polyclonal B cell populations and are subject to phosphorylation at serine residues. Identification of these constituents of the B cell receptor complex opens up the opportunity to study coupling of the B cell antigen receptor to the intracellular signal transduction machinery at the molecular level.
Identification of the genes encoding the IgM‐α and Ig‐β components of the IgM antigen receptor complex by amino‐terminal sequencing
Authors: Hombach Joachim , Lottspeich Friedrich , Reth Michael 
Published: March 2007

AbstractBeside the immunoglobulin (Ig) heavy and light chains the murine B cell receptor of the IgM class contains a heterodimer of two transmembrane proteins (IgM‐α and Ig‐β). By N‐terminal sequencing of IgM‐α and Ig‐β we have identified the genes encoding these proteins as mb‐1 and B29, respectively. Both genes are B cell specific and have been previously cloned from B minus T cell subtractive cDNA libraries. We have constructed expression vectors of the two genes and demonstrate that expression of the mb‐1 and B29 genes can influence the surface expression of IgM in μm‐transfected myeloma cells. From the known sequences of the IgM‐α and Ig‐β proteins and from the results of previous transfection experiments with various vectors expressing the μ chain we have developed a structural model of the B cell antigen receptor of class IgM which we compare with that of the T cell antigen receptor.
Suppression and prevention of adjuvant arthritis in rats by a monoclonal antibody to the α/β T cell receptor
Authors: Yoshino Shin , Schlipköter Eva , Kinne Raimund , Hünig Thomas , Emmrich Frank 
Published: March 2007

AbstractAdjuvant arthritis (AA) in rats is an experimentally induced autoimmune disease mediated by T lymphocytes specific for Mycobacterium tuberculosis. We raised the question whether T cells carrying the γ/δ Tcell receptor (TcR), reactive or not to mycobacterial antigens, are involved in the pathogenesis of AA. For this purpose, T cells bearing the TcR α/β were depleted from circulation by treatment with a monoclonal antibody against the rat TcR α/β (R73). This treatment efficiently suppressed existing disease. Even more efficient was pretreatment with R73 from birth, which prevented AA induction completely. In these α/β+ T cell‐depleted animals an elevated level of α/β− T cells (about 15% vs. 1% in normal rats) was evident, which was not significantly increased by Mycobacterium tuberculosis injection. We found no positive evidence that γ/δ+ T cells do contribute to AA induction. Moreover, treatment with an anti‐TcR α/β monoclonal antibody may be very efficient in treatment of Tcell‐mediated autoimmune diseases.
Selective death of T cell receptor γ/δ+ intraepithelial lymphocytes by apoptosis
Authors: Viney Joanne L. , Macdonald Thomas T. 
Published: March 2007

AbstractIn mice, the majority of Tcells expressing the γ/δ Tcell receptor (TcR) are found at mucosal surfaces, especially the intestinal epithelium. Here we show that in vitro, the majority of TcR γ/δ+ intraepithelial lymphocytes, but not TcR α/β+ intraepithelial lymphocytes, undergo rapid and selective programmed cell death by apoptosis.
Fibronectin facilitates the migration of human natural killer cells
Authors: Somersalo Kristina , Saksela Eero 
Published: March 2007

AbstractThe interaction of lymphocytes with the extracellular matrix plays an important role in the immune defence against tumor cells and virus‐infected cells. We have examined the effect of matrix proteins on the migration of large granular lymphocytes (LGL) through 3‐μm pores in Nuclepore filters in a Boyden invasion chamber. Fibronectin bound on the filter surface significantly increased (p < 0.001) the capacity of LGL to migrate, whereas soluble fibronectin did not. In addition, a significantly higher (p < 0.001) percentage of LGL was capable of migration through fibronectin‐coated filters than through untreated filters. With fibronectin‐coated filters, a strong enrichment of CD16+ and CD56+CD3− cells with LGL morphology and reduction of CD3+ cells was found among migrating cells when the incubation time was 4 h or less. Later agranular lymphocytes, mainly CD3+ T lymphocytes, also started to migrate. Laminin coating of filters also facilitated migration, and when filters were coated with both fibronectin and laminin the increase in migration was equal to the sum of the increases induced by each protein alone. Interactions between cell surface and the Arg‐Gly‐Asp (RGD) peptide sequence of many matrix proteins had no role in the LGL migration through untreated flters. However, when filters were coated with either fibronectin or laminin, or with both, peptide containing the RGD sequence reduced migration to the level of untreated filter, whereas an Arg‐Gly‐Glu control peptide had no effect. Our results show that unstimulated LGL/natural killer cells are capable of rapid migration through matrix‐coated porous membranes, and that interactions between cell surface receptors and the RGD sequence of fibronectin and probably laminin are utilized in this process.
Allelic exclusion of membrane but not secreted immunoglobulin in a mature B cell line
Authors: Picarella Dominic , Serunian Leslie A. , Rosenberg Naomi 
Published: March 2007

AbstractAlthough many B lymphocytes contain two completely rearranged immunoglobulin (Ig) heavy (H) chain genes, only one of the alleles specifies a protein product. This phenomenon is termed allelic exclusion and is controlled in part by the membrane portion of Ig H chains. We have identified a mature B cell line derived from murine bone marrow that expresses two H chain proteins, γ3 and γ2b. Proteins of appropriate size for the membrane and secreted forms of both H chains are produced and both IgG3 and IgG2b are secreted from the cells. However, only IgG3 is expressed on the membrane. Detailed restriction mapping of the H chain genes indicates that both are rearranged, one containing a VHJ558 gene linked to the γ3 constant region and the other a VHS107 gene linked to the γ2b constant region. Primer extension sequencing of the RNA reveals that the γ2b RNA is transcribed from the allele containing VHS107 sequences while the γ3 RNA is transcribed from the allele containing VHJ558 sequences. Thus, this mature B cell line secretes two distinct antibody molecules but is allelically excluded at the level of surface Ig expression. This cell line provides a model system to study factors, in addition to aberrant rearrangement, that influence allelic exclusion.
Signal transduction by HLA class II antigens expressed on activated T cells
Authors: Ødum Niels , Martin Paul J. , Schieven Gary L. , Hansen John A. , Ledbetter Jeffrey A. 
Published: March 2007

AbstractHuman T cells express HLA class II antigens upon activation. Although activated, class II+ T cells can present alloantigens under certain circumstances, the functional role of class II antigens on activated T cells remains largely unknown. Here, we report that cross‐linking of HLA‐DR molecules expressed on allospecific, CD4+ T clones and cell lines can function as transduction elements that trigger rapid cellular responses including tyrosine phosphorylation of cellular proteins and mobilization of Ca2+ from internal stores. The proteins phosphorylated on tyrosine were distinct from those observed after cross‐linking CD4. Ligation of CD4 and class II molecules generated a synergistic effect of the intracellular free Ca2+ concentration response that required an interaction between the molecules on the cell surface. Since class II is the natural ligand for CD4, the present data suggest that class II is induced on activated T cells to regulate CD4 function, possibly by specific interaction with the CD4‐associated p56lck protein tyrosine kinase.
Non‐mitogenic T cell activation signals are sufficient for induction of human immunodeficiency virus transcription
Authors: Gruters Rob A. , Otto Sigrid A. , Al Bert J. M. , Verhoeven Arthur J. , Verweij Cornelis L. , Van Lier René A. W. , Miedema Frank 
Published: March 2007

AbstractCentral Laboratory of the Netherlands Red Cross Blood Transfusion Service and the Laboratory for Clinical and Experimental Immunology of the University of Amsterdem.The expression of human immunodeficiency virus type 1 (HIV) is enhanced after T cell activation due to the interaction of cell‐encoded nuclear factors with binding sites in the viral long terminal repeats (LTR). We studied the minimal signal transduction requirements for induction of HIV transcription during T cell activation. Monoclonal antibodies (mAb) against the T cell receptor/CD3 complex induced interleukin (IL) 2 production as well as HIV‐LTR‐directed gene expression in Jurkat T cells. Addition of cyclosporin A or buffering of intracellular Ca2+ changes did not abolish this LTR‐directed gene expression but did block IL 2 production. In contrast, interference with protein kinase C (PKC) activation did inhibit both IL 2 production and LTR‐driven gene expression. Under all conditions HIV‐LTR‐directed gene expression correlated with gene expression induced by the NF‐kB binding enhancer, but not by the NF‐AT or OCT‐1 binding sites. In accordance with observations by Verweij, Geerts and Aarden on the CD28 co‐stimulatory activation of IL2 transcription via an NF‐kB‐like activity, stimulation of the CD2, CD28 and CD44 accessory molecules was tested to mimick physiological activation signals independent of T cell receptor triggering. mAb directed against CD2 and CD44 only marginally induced the LTR. Next, non‐mitogenic stimulation by mAb against CD28 clearly induced the HIV‐LTR‐ and NF‐kB‐ but not NF‐AT‐ and OCT‐1‐driven chloram‐phenicol acetyltransferase CAT expression, showing a direct effect on gene expression via this receptor.Taken together, this report shows that non‐mitogenic T cell activation signals are sufficient to induce HIV transcription. The finding that these signals may be delivered by receptors that are not dependent on antigen‐specific activation may have important implications for our understanding of HIV pathogenesis.
Morphological features of cloned lymphocytes expressing γ/δ T cell receptors
Authors: Arancia Giuseppe , Malorni Walter , Iosi Francesca , Zarcone Daniela , Cerruti Giannamaria , Favre Anna , Zeromski Jan , Grossi Carlo E. , Moretta Alessandro 
Published: March 2007

AbstractWe have analyzed the morphological characteristics of human T lymphocytes bearing CD3‐associated T cell receptor (TcR) γ and δ chains. BB3 and δ‐TCS1 monoclonal antibodies (mAb) were used to identify two distinct, nonoverlapping populations of TcR γ/δ+ cells which express the products of Vδ2 and Vδ1 gene segments, respectively. In the peripheral blood, most Vδ1+ (δTCS‐1+) lymphocytes express the non‐disulfide‐linked form of receptor whereas Vδ2+ (BB3+) cells express the disulfide‐linked form. The majority of cloned TcR γ/δ+ cells exhibit a growth pattern different from that of conventional TcR α/β+ cells as they adhere promptly to surfaces and undergo morphological changes which can be summarized as follows: cells spread on the surface, form a distinct uropod and, in the final phase of adherence, emit long filopodia ending with adhesion plaques. Immunofluorescence studies of TcR γ/δ+ clones demonstrated the presence of submembranous actin microfilaments and actin‐binding protein confirming that these cells are capable of active motility which is related to the propensity of TcR γ/δ+ cells to home to epithelia.Scanning electron microscope analyses of effector/target cell conjugates showed that in TcR γ/δ+ cells the region of the uropodia next to the cell body is responsible for the binding to tumor target cells. Interestingly, immunofluorescence analyses revealed that LFA‐1 molecules are predominantly distributed in the uropodium whereas they are virtually absent in the cell bodies. These morphological characteristics of TcR γ/δ+ cells may pertain to defensive mechanisms at the mucosal level.
Evidence that the CD45 phosphatase regulates the activity of the phospholipase C in mouse T lymphocytes
Authors: Marvel Jacqueline , Rimon Galia , Tatham Peter , Cockcroft Shamshad 
Published: March 2007

AbstractThe importance of the tyrosine phosphatase CD45 in the regulation of lymphocyte activation was first demonstrated using antibodies against the extracellular domain of CD45 in functional assays. More recently it was reported that CD45‐negative mutants were nonresponsive to stimulation through the T cell receptor‐CD3 complex. We have studied the effect of CD45 cross‐linking on the early signals induced by CD3 in mouse T cells. We show that CD45 cross‐linking inhibits the increase in inositol phosphates and cytoplasmic Ca2+ induced by cross‐linking of CD3. This indicates that CD45 is involved in the regulation of phospholipase C.
L‐Arginine‐dependent destruction of intrahepatic malaria parasites in response to tumor necrosis factor and/or interleukin 6 stimulation
Authors: Nüssler Andreas , Drapier Jean‐Claude , Rénia Laurent , Pied Sylviane , Miltgen François , Gentilini Marc , Mazier Dominique 
Published: March 2007

AbstractThere is growing evidence that cytokines (interleukin [IL] 1, IL 6, interferon‐γ, tumor necrosis factor [TNF]) directly or indirectly interfere with the intrahepatic development of malaria parasites. Recent work in our laboratory clearly showed that TNF can affect the hepatic development of parasites via IL 6 secreted by liver nonparenchymal cells. The possible participation of an L‐arginine‐dependent effector mechanism has been studied to explain the TNF/IL 6‐induced inhibition. We thus investigated if NGmonomethyl‐L‐arginine and Nω‐nitro‐L‐arginine, two specific inhibitors of inorganic nitrogen oxide synthesis from L‐arginine, were able to affect the inhibitory effect of TNF and/or IL 6 in co‐cultures. At 0.1 and 0.5 mM both L‐arginine analogues reversed the inhibitory effect of these cytokines. An interesting observation is that L‐arginine analogues enhance schizont development in the absence of prior cytokine contact. This result indicates an hepatic basal L‐arginine‐dependent anti‐parasitic activity which might explain the existence of self‐degenerating hepatic forms as previously reported.