bluuebunny/crossref_metadata_2025_split huggingface dataset:
Regulation by interleukin 2 of CD23 expression of leukemic and normal B cells: comparison with interleukin 4
Authors: Hivroz Claire , Vallé Alain , Brouet Jean Claude , Banchereau Jacques , Grillot‐Courvalin Catherine 
Published: March 2007

AbstractRecombinant interleukin (IL) 4 has been shown to be able to up‐regulate low‐affinity Fc receptor for IgE (FcεRII)‐CD23 expression on B cells as well as on other human mononuclear cells. We demonstrate here that, in opposition with previous reports, recombinant IL 2 also can up‐regulate CD23 expression on B cells. This was first observed on CLL cells which represent a monoclonal proliferation of B cells arrested at an intermediate stage of activation. Cells of 5 out of 12 B‐CLL studied display such an increase and all 5 proliferated, in vitro, directly in response to IL 2. Similarly, upon triggering with anti‐μ and IL 2, normal tonsillar B lymphocytes also demonstrate an increase of CD23 expression but this was observed only on day 3. Interferon‐γ was able to inhibit this IL 2‐mediated up‐regulation of CD23 on normal B cells but not on CLL‐B cells; on those cells interferon‐γ was similarly unable to inhibit the IL 4‐mediated CD23 up‐regulation. These results suggest that CD23 regulation is complex and related to the stage of activation and the cell type.
Acute rejection of allogeneic hemopoietic progenitors by genetically resistant mice
Authors: Shimamura Kazuo , Kaminsky Steven G. , Nakamura Ichiro 
Published: March 2007

AbstractNatural resistance to hemopoietic allograft results in functional elimination of the graft from the host within 24 to 48 h. The resistance is specific and is directed to the cell surface target structures of an unidentified nature. These determinants are controlled by the major histocompatibility complex‐linked hemopoietic histocompatibility (Hh) loci and expressed by cells of the hemopoietic system. In this study, the susceptibility of various hemopoietic progenitors, as well as the nature and the kinetics of the early rejection process, were examined by directly following the functional survival of the grafted progenitors by periodic sampling. In both F1 hybrid and inbred allogeneic hosts, multipotential progenitors for granulocyte‐erythrocyte‐monocyte‐megakaryocyte lineages, bipotential progenitors for granulocyte‐monocyte lineages and unipotential progenitors of erythrocyte, granulocyte and monocyte were susceptible to elimination. Therefore, within the limited range of comparisons, neither the lineage, nor the degree of commitment or differentiation determines the susceptibility of hemopoietic progenitors to resistance. Functional elimination of the grafted progenitors from the recipient spleen was irreversible upon cultivation in semisolid medium. The frequency of seeding in the spleen at 3 h was comparable in resistant and susceptible hosts elimination commenced shortly afterwards and by 24 h after transplantation < 10% of clonogenic progenitors remained functional. Activation of natural killer cells strengthened pre‐existing resistance, but did not convert genetically susceptible mice to resistant. Therefore, the resistance is dependent on an effector mechanism with predetermined specificity.
Loss of interleukin 2 dependence in cloned interleukin 2‐dependent rat T lymphocyte × BW5147 hybridomas is not associated with segregation of a specific pair of rat chromosomes
Authors: Somoza Chamorro , Fernández‐Ruiz Elena , Jotterand‐Bellomo Martine , Sanz Eva , Nabholz Markus , Silva Augusto 
Published: March 2007

AbstractA fusion between the mouse AKR thymoma BW5147 and a culture of homogeneously OX8+ (CD8) rat T lymphoblasts yield interleukin (IL) 2‐dependent T cell hybridomas when selected in HAT medium supplemented with IL 2‐containing supernatants of concanavalin A‐activated cells and dexamethasone. IL 2‐independent variants can be selected from cloned IL 2‐dependent hybrids in the absence of conditioned medium. Karyotype analysis was used to test a previously proposed hypothesis according to which IL 2‐independent variants arise through loss of a specific cytotoxic T lymphocyte (rat) chromosome carrying a gene responsible for IL 2 dependence. Comparison of karyotypes of several independently derived hybrids with those of their IL 2‐independent variants showed that the hybrids contain at least one homologue of all rat chromosomes, and that no pair of rat chromosomes is consistently absent in the IL 2‐independent variants.
CD15 antibodies increase neutrophil adhesion to endothelium by an LFA‐1‐dependent mechanism
Authors: Forsyth Kevin D. , Simpson Anna C. , Levinsky Roland J. 
Published: March 2007

AbstractAnti‐neutrophil antibodies (CD15) bind to a simple sugar (lactose‐N‐fucopentaose III, LNF III) known to be present on the chains of the adhesion molecules on neutrophils. We have demonstrated that pre‐incubation of neutrophils with a CD15 antibody increases neutrophil adherence to endothelium by a neutrophil‐dependent mechanism. This augmented adhesion can be inhibited by antibodies directed against the α and β chain of the leukocyte function‐associated antigen 1 (LFA‐1) molecule. There is also some increase in surface LFA‐1 expression on neutrophils after CD15 incubation, suggesting that CD15 antibodies increase neutrophil adhesion by an LFA‐1‐dependent mechanism. The increase in LFA‐1 expression after CD15 incubation occurs in the presence of a protein synthesis inhibitor. As LFA‐1 is not stored intracellularly, the increased adherence of the neutrophils, and increased LFA‐1 expression on their surface, suggests the possibility that the CD15 antibodies are binding to the LNF III antigen present on the α and β chains of LFA‐1, producing their effect by activating the molecule, perhaps by exposing new antigen sites by a stearic effect.
Human T cells and interleukin 4 inhibit the release of interleukin 1 induced by lipopolysaccharide in serumfree cultures of autologous monocytes
Authors: Weiss Laurence , Haeffner‐Cavaillon Nicole , Laude Maryline , Cavaillon Jean‐Marc , Kazatchkine Michel D. 
Published: March 2007

AbstractStimulation with lipopolysaccharide (LPS) of unfractionated peripheral blood mononuclear cells in serum‐free cultures resulted in the release of lower amounts of interleukin (IL) 1 as compared with those induced in cultures of purified monocytes. In addition, a dose‐dependent decrease in IL 1 production was observed when purified autologous T cells were added to cultures of LPS‐stimulated monocytes. The inhibitory effect of T cells on IL 1 production was reproduced by adding human recombinant IL4 to monocyte cultures. IL4 optimally inhibited the generation of cell‐associated IL 1 and the extracellular release of IL 1 in monocyte cultures performed in the presence of low doses of LPS. IL 4 inhibited the generation of IL 1 activity and that of IL 1α and IL 1β antigens indicating that IL4 interfered with IL 1 transcription and/or processing rather than induced the synthesis of an IL1 inhibitor. IL2 and IL3 enhanced IL1 production by LPS‐stimulated cells whereas granulocyte‐monocyte colony‐stimulating factor had no effect. IL4 inhibited the production and the release of tumor necrosis factor α activity by monocytes stimulated with LPS. Thus, T cells and IL4 may down‐regulate the production of monokines which induce their proliferation and exert a suppressive effect on the generation of potent proinflammatory mediators.
Monokine production by microglial cell clones
Authors: Righi Marco , Mori Lucia , Libero Gennaro De , Sironi Marina , Biondi Andrea , Mantovani Alberto , Donini Suzanne Denis , Ricciardi‐Castagnoli Paola 
Published: March 2007

AbstractCytokines have been suggested to act as intermediates between the immune and the central nervous system, but little is known about the type of cells synthesizing them in the brain. We have immortalized with oncogenic retroviruses primary brain cell cultures from mouse embryos and have generated clones of microglial cells that have been characterized. Three of the clones studied produce interleukin 1 (IL 1), IL 6 and tumor necrosis factor‐α as assessed by biological assays and by Northern blot analysis. Our data raise the question on the role of these cytokines in the brain and suggest that early resident microglial cells might play an important role in developmental processes and in the adult brain.
MALA‐2, mouse homologue of human adhesion molecule ICAM‐1 (CD54)
Authors: Prieto Jacqueline , Takei Fumio , Gendelman Rita , Christenson Birger , Biberfeld Peter , Patarroyo Manuel 
Published: March 2007

AbstractIn humans, lymphocyte adhesion to cells is mediated by the protein heterodimer CD11a/CD18 (Leu‐CAMa, LFA‐1) and its ligand CD54 (ICAM‐1). Although the murine CD11a/CD18 is well characterized, the mouse homologue of human ICAM‐1 has not been identified. In the present study a rat monoclonal antibody to the murine lymphocyte activation antigen MALA‐2 was found to inhibit in a dose‐dependent manner the phorbol ester‐enhanced aggregation of mouse lymphoblasts, an adhesionspecific assay, and hence to define an adhesion molecule. By immunofluorescence flow cytometry the antigen expression was low on spleen cells but it largely increased after stimulation with mitogens. The antigen was expressed by some, but not all, lymphoid cell lines, and myelomonocytic and mastocytoma cells were also positive. In frozen tissue sections MALA‐2 was mainly detected on germinal center B cells, dendritic cells, macrophages and vascular endothelium, including high endothelial venules. Cell surface labeling followed by immunoprecipitation and gel electrophoresis indicated that the antigen is a sialoglycoprotein which has a relative molecular mass of 95 kDa and displays a faster electrophoretic mobility under nonreducing conditions. The function, cellular distribution and molecular properties of MALA‐2 are indistinguishable from those of human ICAM‐1.
Transcriptional regulation of immunoglobulin expression in a chronic lymphocytic leukemia cell line
Authors: Mårtensson Inga‐Lill , Nilsson Kenneth , Leanderson Tomas 
Published: March 2007

AbstractA cell line derived from a B‐type chronic lymphocytic leukemia, Corinna II, was found to down‐regulate its steady‐state level of IgM mRNA after treatment with phorbol 12‐myristate 13‐acetate while the proliferative capacity of the cell line was unaffected. No changes in the splicing pattern of the IgM transcript could be observed after treatment. The down‐regulatory effect on IgM RNA expression was found to be inhibited by cycloheximide, suggesting that functional protein synthesis was needed for the effect. Transfection experiments showed that the down‐regulatory effect of phorbol myristate acetate was exerted at the level of transcriptional initiation. The DNA element mediating the down‐regulatory effect was found to be present within 140 bp 5' of the mRNA cap site in an immunoglobulin promoter.
Inactivation of rabbit immunoglobulin λ chain variable region genes by the insertion of short interspersed elements of the C family
Authors: Hayzer David J. , Jaton Jean‐Claude 
Published: March 2007

AbstractTwo rabbit germ‐line genes encoding immunoglobulin λ light chain V regions were cloned from a rabbit genomic liver DNA library and characterized. One, Vλ1, is separated by at least 8 kb from any other Vλ gene. The second, Vλ4, forms part of a three‐gene cluster with two functional Vλ genes recently reported. Both Vλ1 and Vλ4 have structural features rendering them pseudogenes. The coding regions have frame‐shift mutations which would yield defective protein products; both genes are also interrupted by the insertions of short, interspersed repetitive elements of the C family. In the Vλ1 gene, the 369‐bp insert is located upstream of the gene between the putative TATA box and the leader exon, whereas in gene Vλ4, the 360‐bp insert interrupts the FR2 at codon 48c. In addition, the sequence of the complement‐determining region 3 of gene Vλ1 is very similar to the mouse DSP2.6 sequence.
Clonal evidence for the induction of NKH1 on activated human thymocytes
Authors: Caligiuri Michael A. , Murray Christine , Levine Herbert , Longtine Janina A. , Ritz Jerome 
Published: March 2007

AbstractFreshly isolated human thymocytes lack the NKH1 antigen and the ability to lyse target cells without major histocompatibility complex restriction. Short‐term culture of human thymocytes in interleukin (IL) 2 results in the generation of non‐major histocompatibility complex‐restricted effector cells, all of which express NKH1. The mechanism by which these cells appear in culture has yet to be elucidated. In the present studies, we developed thymocyte clones and performed a molecular analysis of T cell receptor gene rearrangements to demonstrate that the expression of NKH1 antigen is induced on the surface of NKH1‐ thymocytes in the presence of IL2. In addition, we were able to show that the NKH1+ fraction consistently displayed an increased proliferative response to similar concentrations of IL 2 when compared to NKH1‐ cells, for both clonal and polyclonal populations of thymocytes. Taken together, these studies demonstrate that the initial appearance of the NKH1 antigen following thymocyte culture in the presence of IL2 results from the induction of NKH1 expression on NKH1‐ thymocytes, while the subsequent predominance of this cell type also results from an enhanced proliferative response to IL 2 which coincides with NKH1 expression.
Restricted usage of VH and VX genes by murine monoclonal antibodies against 3‐fucosyllactosamine
Authors: Kimura Hirohisa , Buescher E. Stephen , Ball Edward D. , Marcus Donald M. 
Published: March 2007

AbstractWe are studying the structure and regulation of murine antibodies against the 3‐fucosyllactosamine antigenic determinant. Analysis of the sequences of seven BALB/ c IgM,χ; monoclonal antibodies (mAb), obtained from four fusions, indicates that these antibodies exhibit restriction in their usage of VH and VL genes. Based on a combination of mRNA sequences and Southern filter hybridization data, all seven light chains are encoded by Vχ;24B and Jχ;1 gene segments. Complete mRNA sequences of the heavy chains revealed that all seven mAb are encoded by VH441, six antibodies are encoded by JH4 and one uses a Jn3 gene segment. The VH441 gene segment and all seven mAb contain a potential glycosylation site at Asn 58 in complementarity‐determining region (CDR)2. In contrast to the similarity of the VH regions, the heavy chain CDR3 segments exhibit considerable heterogeneity. They are encoded by three D segments, they vary in length from 7‐9 amino acids and display differences in their deduced amino acid sequences. The VH441 gene segment also encodes antibodies against four other carbohydrate antigens, levan, galactan, dextran and galactosyl globoside. The use of a single gene segment to encode antibodies against five different antigens suggests that the domain encoded by VH441 might be particularly well adapted for forming sites that bind carbohydrate determinants. Glycosylation of CDR2 might contribute to the unique properties of this VH domain.
Non‐random migration of cd4 and cd8 t cells: changes in the cd4: cd8 ratio and interleukin 2 responsiveness of efferent lymph cells following in vivo antigen challenge
Authors: Bujdoso Raymond , Young Patricia , Hopkins John , Allen Deborah , Mcconnell Ian 
Published: March 2007

AbstractIn this investigation we have examined some of the cellular and molecular changes in efferent lymph that drains from an antigen‐stimulated peripheral lymph node. Resting efferent lymph is characterized by a higher percentage of CD4+ cells and consequently, a higher CD4/CD8 ratio than peripheral blood. Following antigen stimulation of a cannulated peripheral lymph node in antigen‐primed sheep, the percentage of CD4+ cells in efferent lymph increases above the resting level during days 1, 2 and 3 post antigen stimulation. This is followed on days, 3, 4, and 5 after antigen stimulation by an increase in the percentage of CD8+ cells above the resting level which occurs as the percentage of CD4+ cells returns to the resting level. These changes cause the CD4/CD8 ratio to first increase above the resting value during the CD4 phase and then decrease below the resting value during the CD8 phase. During the CD4 phase a lymphokine activity is present in cell‐free lymph fluid. Lymph fluid collected at this time supports the proliferation of activated T cells. Supernatants generated from efferent cells collected at a similar time and cultured in vivo for 24 h without any further stimulation are capable of releasing this material. During the CD8 phase cells expressing functional interleukin(IL) 2 receptors appear in lymph fluid. The data suggests a sequential exit of T cell subsets from an antigen‐stimulated lymph node and that the appearance of IL 2‐like activity and IL 2‐responsive cells in efferent lymph fluid are temporally distinct events.
Bioactive human recombinant tumor necrosis factor‐α: an unstable dimer?
Authors: Petersen Claus Munck , Nykjær Anders , Christiansen Brian S. , Heickendorff Lene , Mogensen SøRen C. , Møller Bjarne 
Published: March 2007

AbstractAs determined by native polyacrylamide gel electrophoresis (PAGE) and gel chromatography the molecular mass of native tumor necrosis factor (TNF)‐α was approximately 35 kDa. When incubated at low concentrations (< 1 nM) 125I‐labeled TNF‐α and unlabeled TNF‐α rapidly multimerized or dissociated into monomers and bioactivity decreased. Sodium dodecyl sulfate (SDS)‐PAGE analysis of cross‐linked 125I‐labeled TNF‐α demonstrated bands of multi‐ and trimeric TNF‐α in addition to dominating bands of dimers and monomers. Tri‐, di‐ and monomeric TNF‐α were recovered from SDS‐PAGE gels and allowed to renature. Of the original receptor‐binding activity, 10%–15% was obtained with cross‐linked TNF‐α dimers, whereas none was recovered from preparations of trimeric TNF‐α. Multimeric and monomeric TNF‐α exhibited little or no binding activity, and cell‐bound, cross‐linked TNF‐α which was dissociated from cellular binding sites was mainly dimeric. 125I‐labeled TNF‐α bound to lymphokine‐activated killer (LAK) cells and binding kinetics were much similar (Kd approximately 100 pM) to those reported in other normal cell types. The number of receptors per LAK cell was approximately 4 × 103. Cross‐linking of TNF‐α to binding sites in U‐937 and LAK cells yielded a receptor‐ligand complex of about 80/90 kDa. At 37 °C, 125I‐labeled TNF‐α was rapidly internalized and degraded in L‐929, U‐937 and LAK cells. Degradation of ligand and recycling of receptors were blocked in the presence of methylamine. Methylamine significantly inhibited TNF‐α‐mediated cytolysis of L‐929 cells and caused a quantitatively corresponding reduction in cellular TNF‐α uptake, indicating that L‐929 lysis was mediated by receptors.
Effects of lipopolysaccharide on macrophages analyzed with anti‐lipid A monoclonal antibodies and polymyxin B
Authors: Lasfargues AgnÈS , Tahri‐Jouti Mohamed‐Ali , Pedron Thierry , Girard Robert , Chaby Richard 
Published: March 2007

AbstractSix monoclonal antibodies (mAb) to the lipid A region of bacterial lipopolysaccharide (LPS), obtained from mice immunized with lipid A‐coated Bordetella pertussis cells (mAb 3.E8, 2.21, 2.37, 2.41) or with lipid A covalently coupled to keyhole limpet hemocyanin (mAb R1 and R7), were examined for their potential to inhibit in vitro activities of LPS on macrophages. mAb R7 was inactive in vitro, but the five other mAb inhibited efficiently some in vitro activities of LPS. mAb R1, 2.21 and 3.E8 reduced the LPS‐induced secretion of tumor necrosis factor (TNF) and interleukin 1 (IL 1) by macrophages, but did not modify the binding of LPS to macrophages. On the other hand, mAb 2.37 and 2.41 reduced LPS binding to macrophages and subsequent IL 1 secretion, but did not modify TNF production. This is in agreement with our previous finding that IL 1 and TNF productions can be selectively triggered by synthetic analogs of lipid A substructures (Lasfargues and Chaby, Cell. Immunol. 1988. 115: 165). The pattern of in vitro inhibition of LPS activities (LPS binding to macrophages and production of TNF and membrane IL 1) by polymyxin B was different from those of the two groups of anti‐lipid A mAb mentioned above. These observations suggest the presence on lipid A of four functionally distinct substructures.
Anti‐inflammatory activity of human IgA antibodies and their Fabα fragments: inhibition of IgG‐mediated complement activation
Authors: Russell Michael W. , Reinholdt Jesper , Kilian Mogens 
Published: March 2007

AbstractThe interaction of human IgA antibodies with the classical pathway of complement activation was investigated in a homologous human system, by means of two IgA1 and three IgG1 myeloma proteins having antibody activity against a defined antigen, staphylococcal α‐toxin. In a solid‐phase antigendependent C3b‐binding ELISA system, the monoclonal IgG antibodies were previously shown to activate the classical complement pathway synergistically, resembling polyclonal IgG antibodies, whereas IgA antibodies were unable to activate complement by either pathway. In the present study, IgA antibodies were found to inhibit significantly the activation of complement initiated by antigenbound polyclonal or mixed monoclonal IgG antibodies, in relation to the amount of IgA antibodies applied and bound to antigen. IgA1 myeloma proteins devoid of antigen‐binding activity were without effect. Inhibition was independent of the ability of the IgA antibodies to compete against the IgG antibodies in binding to antigen, and was demonstrable with physiological concentrations of antibodies. Similar results were obtained with polyclonal serum IgA having antigen‐binding activity. However, the binding of C1q to antigen‐complexed IgG was inhibited only by a monoclonal IgA antibody that could compete against one of the three monoclonal IgG antibodies that bound C1q synergistically. This observation implied that at least two mechanisms were involved in the inhibition of C3b fixation. Fabα fragments of monoclonal IgA antibodies, obtained by cleavage with IgA1 protease from Haemophilus influenzae type b, were found to have a similar inhibitory effect on C3b fixation to the intact IgA1 antibodies. This observation supports the hypothesis that IgA1 proteases contribute to the invasive pathogenicity of certain mucosal bacteria, by cleaving secretory IgA1 antibodies to antigen‐binding Fabα fragments, which are not only defective in mucosal defense properties, but which also protect the organisms from other immune effector systems, such as complement activation.