bluuebunny/crossref_metadata_2025_split huggingface dataset:
Binding of monomeric immunoglobulins by bone marrow‐derived mononuclear phagocytes; its modulation by interferon‐γ
Authors: Keller Robert , Keist Ruth , Bazin Hervé , Joller Peter , van Der Meide Peter H. 
Published: March 2007

AbstractThe ability of resting and activated rat bone marrow‐derived mononuclear phagocytes (BMMΦ) to bind monomeric rat, mouse, and human IgG was determined by means of flow cytometry. Rat IgG2b bound with high affinity (Kd ≅ 3 × 10−9); binding was optimal at 4°C and was only little affected by trypsin treatment. The other IgG bound with only low affinity (rat IgG2a, mouse and human IgG) or not at all to rat BMMΦ (rat IgG1, rat IgG2c). The binding of rat IgG2b was not affected by the presence of a surplus of low‐affinity binding IgG, and vice versa, indicating that high‐ and low‐affinity IgG bind to different sites. Binding of high‐ and low‐affinity IgG as well as expression of MHC class II molecules and of tumoricidal activity by BMMΦ was markedly enhanced by rat interferon‐γ in low concentration (0.1 to 1.0 IU IFN‐γ/ml). On the other hand, heat‐killed Corynebacterium parvum organisms, that were equally potent in triggering tumoricidal activity, neither enhanced the binding of IgG nor the expression of MHC class II molecules by BMMΦ, suggesting that these abilities are not necessarily closely related phenomena.
Exposure of female mice to type II collagen reduces susceptibility to collagen‐induced arthritis in offspring
Authors: van Vollenhoven Ronald F. , Thorbecke G. Jeanette , Siskind Gregory W. 
Published: March 2007

AbstractThe effect of exposure of female DBA/1 mice to collagen II (CII) prior to breeding on the susceptibility of their offspring to CII‐induced arthritis (CIA) was investigated. It was found that female offspring, born within 3 months after exposure of the mothers to CII, had a significantly reduced incidence of CIA, following immunization with CII. Just prior to this immunization, no anti‐CII could be detected in the offspring. Offspring born more than 3 months after exposure of the mothers to CII showed no differences in susceptibility to induction of CIA, if optimal conditions for induction were used. However, when suboptimal conditions for induction of CIA were used, offspring of females that had been exposed to CII developed less severe arthritis and had a delayed onset of arthritis as compared with controls. It is concluded that exposure of female mice to CII prior to mating results in changes in the immune response to CII in the offspring, leading to a subtle decrease in susceptibility to CIA.
The influence of S17 stromal cells and interleukin 7 on B cell development
Authors: Cumano Ana , Dorshkind Kenneth , Gillis Steven , Paige Christopher J. 
Published: March 2007

AbstractA clonal assay was used to study different stimuli involved in the progression of fetal liver B cell precursors to mature B lymphocytes.In this report we replaced fetal liver heterogenous feeder cells by a recombinant growth factor, interleukin 7 (IL 7), and a clonal stromal cell line, S17. Under those conditions we could clone 1 in 10 B220+ B cell precursors from fetal liver and the cells could differentiate to a mitogen‐responsive, immunoglobulinsecreting stage. We found that IL 7 stimulates proliferation of B220+ precursors but is not sufficient to support maturation of those precursors to a stage of mitogen responsiveness. We show further that the cell line S17 does not produce IL 7 at functionally detectable level but provides support for B cell maturation. We conclude that this cell line supplies an exogenous stimulus required by B cell precursors to become mature lymphocytes. We describe therefore two stages in pre‐B cell development: (a) IL 7‐dependent proliferation and (b) S17‐dependent maturation to mitogen reactivity. Further studies demonstrate that S17 has a profound effect on B cells by increasing the clonal efficiency of lipopolysaccharide‐responsive cells to nearly 1:1 B cell in the spleen of adult C57BL/6 mice.
A new surface antigen on intraepithelial lymphocytes in the intestine
Authors: Kilshaw Peter J. , Murant Susan J. 
Published: March 2007

AbstractA new surface molecule has been discovered on mouse intestinal intraepithelial lymphocytes (IEL) using a rat anti‐mouse IEL monoclonal antibody, M290. It was expressed at high levels on nearly all IEL and on a majority of T cells in the gut lamina propria. M290 stained, with lower intensity, a small minority of T cells in other lymphoid tissues. Expression was biased towards the CD8+ subset. Stimulation of peripheral T cells with mitogens did not induce expression of the new antigen but addition of transforming growth factor β to stimulated T cells had a marked inductive effect. Sodium dodecyl sulfate‐polyacrylamide gel electrophoretic analysis of IEL surface components precipitated with M290 showed principal bands at 135, 120, 28 and 24 kDa (reduced) and 135, 100, 24 and 21 kDa (nonreduced). Precipitation with antibodies to integrin subunits showed that the new molecular complex was not a member of the β1, β2, or β3 integrin families although all of these were represented on IEL. A 13‐amino acid N‐terminal sequence obtained from the 120‐kDa β subunit of the antigen prepared from an M290+ Thybridoma (MTC‐1) did not show homology with integrins. Pulse‐chase studies using MTC‐1 cells showed that the 135‐kDa α subunit was derived from a 147‐kDa precursor. The function of this new molecular complex is not yet known.
Induction of antibody synthesis by CD4+ T cells: IL 5 is essential for induction of antigen‐specific antibody responses by TH2 but not TH1 clones
Authors: Dekruyff Rosemarie H. , Mosmann Rim R. , Umetsu Dale T. 
Published: March 2007

AbstractMurine B cells stimulated with lipopolysaccharide (LPS) and interleukin (IL) 4 produce IgG1 and IgE, but synthesize IgG2a when stimulated with LPS and interferon‐γ. The cytokines, however, that regulate immunoglobulin (Ig) synthesis induced in normal B cells under antigen‐driven major histocompatibility complex (MHC)‐restricted conditions in the absence of potent B cell mitogens have not been fully elucidated. We and others have shown that under cognate MHC‐restricted conditions, CD4+ T cell clones of the TH1 subset, which produce IL 2 and interferon‐γ, and T cell clones of the TH2 subset, which produce IL 4 and IL 5, are both capable of inducing anti‐trinitrophenyl IgG plaque‐forming cells. In this report we have examined in further detail the cytokine requirements for the induction of Ig synthesis in B cells cultured directly with TH1 and TH2 T cell clones.Using (a) TH2 clones that varied in the amount of IL 5 secreted, (b) a neutralizing monoclonal antibody against IL 5 and (c) T cell clones pretreated with cyclosporin A to inhibit cytokine secretion, we found that IL 5 was essential for induction of IgG1 synthesis by TH2 but not TH1 T cells. Although we demonstrated that IL 2 could actually up‐regulate the synthesis of IL 5 by TH2 clones, the induction of IgG synthesis by TH2 clones was entirely independent of IL 2. In contrast, induction of IgG1 synthesis by TH1 clones was absolutely dependent upon the presence of IL 2 and was not affected by the presence of IL 5. Thus, these studies demonstrate the idea that at least two independent pathways exist for the induction of IgG1 synthesis, and that one of these pathways is IL 4/IL5 dependent and the other IL 2 dependent.
Molecular associations on the T cell surface correlate with immunological memory
Authors: Dianzani Umberto , Luqman Mohammad , Rojo Jose , Yagi Junji , Baron Jody L. , Woods Andrea , Janeway Charles A. , Bottomly Kim 
Published: March 2007

AbstractDifferent isoforms of CD45 are expressed on naive and memory CD4 T cells in the mouse, as revealed by an antibody to a set of isoforms of CD45 that utilize exon B, called CD45RB. Cloned TH1 and TH2 lines also differ for expression of isoforms detected by this antibody. Differential expression of CD45 isoforms correlates with different behavior of cell surface molecules involved in transmembrane signal transduction. On naive T cells, CD4, CD45 and the CD3/T cell receptor complex behave as independent entities. On memory T cells, these three molecules are stably associated on the T cell surface. Furthermore, on TH2 cells, which express intermediate levels of CD45RB, CD4 is stably associated with CD45 isoforms other than CD45RB, but this complex is not associated with the CD3/T cell receptor. These results lead us to propose that immunological memory in CD4 T cells consists of an altered structure of the T cell's specific signal transduction apparatus controlled by low‐molecular weight CD45 isoforms. This altered receptor structure would allow the more sensitive triggering of the T cell characteristic of memory cells. The organization of multimolecular signal transduction systems may be a general means by which cells alter their physiological behavior, allowing the acquisition of new phenotypic characteristics.
Suppression of B cell activation by cyclosporin A, FK506 and rapamycin
Authors: Wicker Linda S. , Boltz Robert C. , Matt Victoria , Nichols Elizabeth A. , Peterson Laurence B. , Sigal Nolan H. 
Published: March 2007

AbstractThe effects of the immunosuppressants cyclosporin A (CsA), FK506 and rapamycin have been compared using murine B cells activated with a variety of mitogens. FK506 is a macrolide antibiotic that has been recently shown to inhibit T cell activation by a mechanism that appears similar to that of CsA. Rapamycin is a macrolide structurally related to FK506 whose mechanism of T cell suppression appears to be distinct from that of FK506 and CsA. While CsA and FK506 were found to preferentially inhibit B cell activation caused by stimuli which induce a rise in intracellular calcium, rapamycin partially inhibited activation by all stimuli tested, including those which are not associated with a calcium flux. All three compounds were found to inhibit cell cycle progression within the G1 phase; however, the rapamycin‐sensitive event within G1 was completed earlier than the G1 events inhibited by CsA and FK506. In addition, inhibition of anti‐IgM‐activated B cells with CsA and FK506, but not with rapamycin, resulted in cell death. These data suggest that although CsA, FK506 and rapamycin are all inhibitors of B cell activation, the inhibitory activity of rapamycin can be clearly distinguished from that of CsA and FK506.Although the suppressive effects of CsA and FK506 on B cell proliferation were nearly identical in this study, their biological activities were distinguishable since FK506, but not CsA, could antagonize rapamycin‐mediated suppression.
Protective methylation of immunoglobulin and T cell receptor (TcR) gene loci prior to induction of class switch and TcR recombination
Authors: Burger Christa , Radbruch Andreas 
Published: March 2007

AbstractMethylation of the Sγ1 switch region and Cγ1 constant region gene from the immunoglobulin heavy chain locus and of the Jβ2 and Cβ regions from the T cell receptor β chain (TcRβ) locus is compared here in murine germ‐line cells, nonlymphoid cells and lymphocytes. In germ‐line cells and in lymphocytes prior to recombination all four regions show strong methylation, i.e. most MspI sites are methylated. After activation of lymphocytes, demethylation is observed for those regions which are activated for recombination, at specific sites 5′ of Sγ1 in B cells activated with bacterial lipopolysaccharide and interleukin 4, and for Jβ2 in thymocytes. In nonlymphoid cells, where these regions cannot be used for recombination, considerable demethylation is observed for all four regions analyzed as compared to lymphocytes. The result implies an important role for methylation of recombinatorial regions. Methylation may be involved in protecting them from uninduced recombination, thus allowing regulated expression of distinct genes in lymphocyte ontogeny.
Functional characterization of the antibody‐mediated protection against blood stages of Plasmodium falciparum in the monkey Saimiri sciureus
Authors: Groux Hervé , Perraut Ronald , Garraud Olivier , Poingt Jean Philippe , Gysin Jürg 
Published: March 2007

AbstractThe squirrel monkey Saimiri sciureus is one of the World Health Organization recommended experimental models of Plasmodium falciparum blood stage infection. Anti‐malaria antibodies developed by this host after a drug‐controlled infection play an important part in the acquired protection against the P. falciparum blood stages. Futhermore, the use of two anti‐Saimiri immunoglobulin (Ig) monoclonal antibodies (mAb) has permitted the differentiation between protective (mAb 3A2/G6) and non‐protective (mAb 3E4/H8) antibodies, as shown by transfer experiments to recipient monkeys infected with blood stage parasites. In the present study we have established that protection conferred by the 3A2/G6+ protective Ig preparation is strictly associated with an in vitro opsonic activity. Such an opsonic activity is not detectable in the 3E4/H8+ non‐protective Ig population. In addition, results indicate that the 3E4/H8+ non‐protective Ig population competes with protective opsonic 3A2/G6+ Ig antibodies when co‐incubated with parasitized red blood cells. Thus, it follows that protection can be directly correlated to the quantitative and qualitative fluctuation of the two Ig populations. When challenged with 1 × 108 P. falciparum‐infected Saimiri red blood cells parasitemia occurred in 5 out of 12 Saimiri who were lacking detectable 3A2/G6+ opsonic antibodies in their sera. By employing antibodies against the human Fc receptor for IgG (FcγR) in an in vitro phagocytic assay, we have been able to show that the principal receptor is FcγRIII. Finally, we also show that in contrast to the situation in man, this receptor is present on circulating monocytes. These findings could lead to a different strategy in designing malaria vaccine candidates and also allow the possibility of predicting the outcome of immunization trials in Saimiri monkeys.
Generation of hen egg lysozyme‐specific and major histocompatibility complex class I‐restricted cytolytic T lymphocytes: recognition of cytosolic and secreted antigen expressed by transfected cells
Authors: Forquet Fréderique , Calin Véronique , Trescol‐Biemont Marie‐Claude , Kanellopoulos Jean , Mottez Estelle , Kourilsky Philippe , Rabourdin‐Combe Chantal , Gerlier Denis 
Published: March 2007

AbstractSyngeneic cells exogenously supplied with hen egg lysozyme (HEL) or endogenously synthesizing HEL were used as antigen‐presenting cells to induce major histocompatibility complex class I‐restricted cytotoxic T lymphocytes (CTL). Immunization of C57BL/6 mice followed by repeated stimulation of their splenocytes in vitro with trypsinized HEL peptides led to the generation of CTL lines specific for trypsinized HEL peptides and restricted by H‐2Kb. Immunization of C3H mice with a mixture of soluble native HEL and irradiated syngeneic spleen cells followed by in vitro stimulation of immune spleen cells with soluble HEL could in a few cases result in HEL‐specific CTL able to kill syngeneic transfectant L cells secreting HEL (HELs) or expressing cytosol‐targeted HEL (HELc). The use of HELs or HELc transfectant L cells as in vivo and in vitro immunogens was a potent way for eliciting HEL‐specific polyclonal CTL. These CTL and two CD8+ clones were found to be H‐2Kk restricted and specific for the 1‐17 N‐terminal HEL peptide. In addition, the anti‐HEL CTL could also exhibit a significant cross‐reactivity against unsensitized and HEL‐untransfected targets expressing the K restriction element. This cross‐reactivity was likely due to recognition of unidentified HEL mimicking peptides (self‐derived ?) presented by the MHC class I (H‐2Kb or H‐2Kk) molecule used as the restriction element for the specific recognition of HEL. The CTL raised after immunization with HELs or HELc transfectant cells were found to recognize both the HELs and HELc transfectant cells even though HEL was not detected in the latter after a 2‐ or 5‐min radiolabeling pulse. Recognition of both HELs and HELc transfectant cells by a given CTL clone suggests that HEL subjected to two separate processing pathways, each depending on the initial subcellular localization, can ensure the generation of similar MHC class I peptide complexes.
Leukocyte function‐associated antigen 1 (LFA‐1) is a signaling molecule for cytoskeletal changes in a human T cell line
Authors: Kelleher Dermot , Murphy Anne , Cullen Derek 
Published: March 2007

AbstractThe HuT 78/2 clone is a human T cell clone which has an activated phenotype. When this line was stimulated with immobilized antibody to LFA‐1, the majority of cells developed dendritic processes. These processes were demonstrated to contain cytoskeletal elements including microtubules and intermediate filaments. Phorbol myristate acetate synergized with and prolonged this effect. Thus, the LFA‐1 molecule may function as a signaling molecule for cytoskeletal reorganization in a human T cell clone.
Microenvironmental organization and stromal cell associations of B lymphocyte precursor cells in mouse bone marrow
Authors: Jacobsen Karen , Osmond Dennis G. 
Published: March 2007

AbstractB lymphocyte precursor cells expressing B220 glycoprotein have been examined in mouse bone marrow (BM) by the in vivo binding of monoclonal antibody (mAb) 14.8 visualized by light and electron microscope radio autography. Young mice were injected intravenously with 125I‐labeled mAb 14.8 and then perfused to remove unbound antibody. Quantitative analysis of radioauto graphic sections of femoral BM revealed many labeled mAb 14.8‐binding cells which were situated both singly and in groups throughout the extravascular BM parenchyma. Groups of large 14.8+ cells were located in patchy areas in the peripheral regions of the BM near the endosteum. These cells were shown to include proliferating precursor B cells by using mice given vincristine sulfate to stop cells in metaphase and mice treated from birth with anti‐IgM antibodies to delete mature B lymphocytes. Electron microscopy revealed clusters of 14.8+ cells intimately associated with the processes of stromal reticular cells. Other 14.8+ cells were in close contact with macrophages; in some instances the intervening cell membranes were indistinct and the macrophages contained 14.8+ material in their cytoplasm. In addition, 14.8+ small lymphocytes were highly concentrated within the lumen of some sinusoids. The present method of detecting B lineage precursor cells in situ has led to a working model of the microenvironmental organization of primary B cell genesis in vivo. The model proposes (a) a centrally directed sequence of differentiation initiated by early precursor cells situated peripherally near the surrounding bone; (b) close associations between precursor B cells and stromal reticular cells; (c) deletion of ineffective B cells by macrophages, and (d) an intravascular maturation phase before B lymphocytes are finally delivered into the blood stream.
Molecular cloning and characterization of WP34, a phosphorylated human lymphocyte differentiation and activation antigen
Authors: Kumar Kadiyala R. , McIntyre Bradley W. , Krensky Alan M. 
Published: March 2007

AbstractAn absorbed antiserum was made by incubating a cytotoxic T lymphocyte immune antiserum with the T cell leukemia HPB‐ALL, thus removing reactivity to known lymphocyte function‐associated antigens. This antiserum was used to screen a cDNA expression library and isolate a novel human lymphocyte cDNA clone designated WP34. WP34 transcript is expressed in functional T cells and a variety of hematopoietic cell lines and tissues, including fetal liver and thymus, but not in HPB‐ALL or any non‐hematopoietic cell lines or tissues tested. The WP34 protein is an acidic, phosphorylated molecule with a pI of 4.5 and molecular mass of 50 kDa. WP34 protein expression is absent in resting peripheral blood lymphocytes but can be induced with antigen stimulation, while the transcript is constitutively expressed. Sequence analysis indicates that WP34 is the human homologue of the recently described murine molecule LSP1.
Glucocorticoids inhibit the production of IL 6 from monocytes, endothelial cells and fibroblasts
Authors: Waage Anders , Slupphaug Geir , Shalaby Refaat 
Published: March 2007

AbstractWe have examined the effect of dexamethasone (DM) and cortisol on the production of interleukin (IL)6 from the murine macrophage cell line RAW 264.9, human monocytes, human endothelial cells and the human fibroblast cell line FS4. In RAW 264.9 cells DM in the concentration range 10−9 M to 10−6 M inhibited the lipopolysaccharide (LPS)‐induced production of IL 6 by 10% to 90%. Cortisol had a similar effect, but was about 25 times less potent than DM. Also, when 10−6 M of DM was added to the cultures after addition of LPS, it completely inhibited the residual 24‐h production of IL 6. Corresponding to the effect on IL 6 production, DM (10−6 M) reduced the mRNA levels for IL 6 in the RAW 264.9 cells. The glucocorticoid analogue RU 486 competes with DM and cortisol for the glucocorticoid receptor and reversed the inhibitory effect of DM, demonstrating that DM exerts its effect via the glucocorticoid receptor. DM also had an inhibitory effect on LPS‐stimulated IL 6 production in freshly isolated human monocytes, and on IL 1‐stimulated IL 6 production in human endothelial cells and FS4 fibroblasts. These results demonstrate that DM via a receptormediated mechanism inhibits IL 6 production at the transcriptional level, and this may contribute to the anti‐inflammatory and immunosuppressive effect of glucocorticoids.
Decreased accessory cell function of macrophages after infection with human immunodeficiency virus type 1 in vitro
Authors: Ennen Joachim , Seipp Inka , Norley Stephen G. , Kurth Reinhard 
Published: March 2007

AbstractPeripheral blood monocytes from human immunodeficiency virus (HIV)‐infected individuals or AIDS‐related complex/AIDS patients ex vivo exhibit distinct alterations in some but not all immune functions. In studies presented here, monocytes from healthy donors were infected with HIV 1 in vitro and co‐cultures with autologous uninfected T lymphocytes were set up. The monocyte/macrophage (MΦ)‐dependent T cell function was determined by measurement of proliferative and secretory [interleukin (IL)2, interferon‐γ] responses to lectin (phytohemagglutinin), mitogen (anti‐CD3 monoclonal antibody), or recall antigen (tetanus toxoid, tuberculin). Accessory function of MΦ was normal after HIV infection when optimal amounts (10%–20%) were added to the T lymphocytes. However, HIV infection of MΦ significantly decreased T cell proliferative responses and secretion of IL 2 when supplemented at limited dilution (0.5%‐5%), although interferon‐γ production was not affected. Whereas the lipopolysaccharide‐triggered MΦ production of IL 1 was not impaired by HIV 1 infection, there was a significant decrease in this response when anti‐CD3 monoclonal antibody or tetanus toxoid were used to trigger the peripheral blood mononuclear cells. The impairment of proliferation of T lymphocytes in the presence of HIV 1‐infected MΦ could be overcome by addition of exogenous IL 1. Taken together, these data clearly show that the mononuclear phagocytedependent enhancement of stimulated T cell proliferation and lymphokine secretion is decreased when the restricted numbers of monocytes/MΦ are HIV 1 infected. There are, therefore, two possible roles of MΦ in HIV infection and progression to disease. First, as a reservoir and vehicle for dissemination of the virus, and second, as an immune cell whose essential functions are impaired by infection.