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Results for “Immunologic Capping”

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At least 613 records · Page 34Linked to original sources
PubMed1998

Mammalian Polycomb group genes are categorized as a new type of early response gene induced by B-cell receptor cross-linking.

Polycomb group (PcG) genes were initially described in Drosophila melanogaster as regulators of the homeobox gene. Four mammalian homologues, mel-18, bmi-1, M33 and rae-28, are analyzed in this study. They not only regulate mammalian homeotic genes by analogy with their Drosophila counterparts, but also have some influence on the growth and differentiation of B lymphocytes. Here we report that these four mammalian PcG genes are rapidly induced after antigen-receptor cross-linking in B cells. Thus we would like to propose that mammalian PcG genes can be categorized as a new type of immediate early gene.

Animals↗
PubMed1981

Roles of influenza virus infectivity and glycosylation of viral antigen for recognition of target cells by cytolytic T lymphocytes.

The influenza virus strains A/JAP (H2N2) and the recombinant strain A/JAP/BEL (H2N1) were tested before and after UV-light inactivation for their ability to sensitize target cells for cytotoxic T-cell lysis (CTL). Infectious preparations were efficient sensitizers for both specific and cross-reactive CTL, exposure of the cells to even low doses of virus resulting in almost maximum susceptibility. When inactivated, however, A/JAP/BEL was about 10 times more efficient than A/JAP at sensitizing the cells for specific CTL; neither sensitized the cells for cross-reactive CTL. Thus factors other than or in addition to a cleaved haemagglutinin (HA) molecule are important in the fusion of the virus with the cell membrane. Target cells which were infected with virus and exposed to different concentrations of tunicamycin, which inhibits glycosylation, became susceptible to CTL by both specific and cross-reactive effector cells through to a lesser extent than controls. Infected cells showed both strong haemadsorption and cocapping of the HA with K, D gene products. Both of these properties were greatly diminished in the presence of even low concentrations of tunicamycin. Analysis of binding studies using labelled monoclonal anti-HA IgG showed that, in the presence of tunicamycin, the total amount of HA expressed at the cell surface was not reduced, but there was an increase in the dissociation constant of the reaction between expressed HA and antibody. This latter finding was thought to reflect a conformational change in the HA antigen, which might be the reason for the reduced susceptibility to CTL.

Animals↗
PubMed1999

Influence of microgravity on mitogen binding and cytoskeleton in Jurkat cells.

The effects of microgravity on Jurkat cells--a T-lymphoid cell line--was studied on a sounding rocket flight. An automated pre-programmed instrument permitted the injection of fluorescent labelled concanavalin A (Con A), culture medium and/or fixative at given times. An in-flight 1 g centrifuge allowed the comparison of the data obtained in microgravity with a 1 g control having the same history related to launch and re-entry. After flight, the cells fixed either at the onset of microgravity or after a or 12 minute incubation time with fluorescent concanavalin A were labelled for vimentin and actin and analysed by fluorescence microscopy. Binding of Con A to Jurkat cells is not influenced by microgravity, whereas patching of the Con A receptors is significantly lower. A significant higher number of cells show changes in the structure of vimentin in microgravity. Most evident is the appearance of large bundles, significantly increased in the microgravity samples. No changes are found in the structure of actin and in the colocalisation of actin on the inner side of the cell membrane with the Con A receptors after binding of the mitogen.

Actins↗
PubMed1999

CD72-deficient mice reveal nonredundant roles of CD72 in B cell development and activation.

CD72, a B cell surface protein of the C-type lectin superfamily, recruits the tyrosine phosphatase SHP-1 through its ITIM motif(s). Using CD72-deficient (CD72-/-) mice, we demonstrate that CD72 is a nonredundant regulator of B cell development. In the bone marrow of CD72-/- mice, there was a reduction in the number of mature recirculating B cells and an accumulation of pre-B cells. In the periphery of CD72-/- mice, there were fewer mature B-2 cells and more B-1 cells. In addition, CD72 is a negative regulator of B cell activation, as CD72-/- B cells were hyperproliferative in response to various stimuli and showed enhanced kinetics in their intracellular Ca2+ response following IgM cross-linking.

Animals↗
PubMed1999

Ig-alpha cytoplasmic truncation renders immature B cells more sensitive to antigen contact.

To study the function of Ig-alpha in the selection of autoreactive B cells, we have analyzed mb-1 cytoplasmic truncation mutant mice (mb-1delta(c)/delta(c)), which coexpress transgenes encoding hen egg lysozyme (HEL) and HEL-specific immunoglobulin. We demonstrate that in the presence of soluble HEL (sHEL) and dependent on the mb-1delta(c) mutation, most immature B cells bearing the HEL-specific Ig transgene undergo rearrangements of endogenous kappa light chains, resulting in loss of HEL specificity. Moreover, immature B cells from Ig-alpha mutant mice respond to BCR cross-linking with an exaggerated and prolonged calcium response and induction of protein tyrosine phosphorylation. Our data imply a negative signaling role for Ig-alpha in immature B cells.

Animals↗
PubMed2001

Regulation of human intestinal mast cells by stem cell factor and IL-4.

Mature human mast cells are tissue-residing, key effector cells of immediate allergic reactions. Moreover, mast cells have been recognized as a potent cellular source of multiple cytokines, suggesting an important role in immunoregulation and host defense. Here, we report on the regulation of mature human mast cells isolated from intestinal tissues by stem cell factor (SCF) and interleukin (IL)-4. SCF is substantially necessary for mast cell survival and induces marginal mast cell proliferation in vitro, whereas IL-4 by itself has no effects on mast cell survival or proliferation. Most interestingly, in synergy with SCF, IL-4 strongly enhances mast cell proliferation. In the presence of SCF, mast cells predominantly produce pro-inflammatory cytokines including tumor necrosis factor (TNF)-alpha, IL-1beta, IL-6, IL-8, IL-16, and IL-18. Addition of IL-4 to the culture medium induces the expression of Th2-type cytokines (IL-3, IL-5 and IL-13), and a downregulation of pro-inflammatory cytokines, namely IL-6. Furthermore, SCF by itself supports the predominance of the tryptase/chymase double-positive mast cell subtype MCTC whereas the addition of IL-4 supports the chymase negative MCT subtype. In conclusion, SCF may primarily regulate resident mast cell survival, whereas IL-4 may promote local proliferation of mast cells and their expression of Th2-type cytokines.

Cell Division↗
PubMed1980

Lateral mobility of integral membrane proteins is increased in spherocytic erythrocytes.

Alterations of glycoprotein distribution and lateral mobility in cell membranes can provide transmembrane signals for several membrane-related phenomena. Control of the transmembranous events has been ascribed to interaction between submembranous protein matrices (or 'cytoskeletons') and membrane glycoproteins. A consequence of such interaction would be differential inhibition of protein lateral diffusion in biological membranes. Measurements of the lateral diffusion coefficients of membrane proteins, in fact, have generally yielded values much less than were predicted for unhindered diffusion in a fluid bilayer. The mouse spherocytic erythrocyte, which lacks the major components of the normal erythrocyte membrane matrix (composed of spectrin, actin, bands 4.1 and 4.9 (ref. 16), in the nomenclature of Fairbanks et al.), provides a unique system for a direct evaluation of the effect of the matrix on protein lateral mobility. After using a modification of the technique of fluorescence redistribution after photobleaching (FRAP), we report here that membrane proteins diffuse about 50 times faster in spherocytic than in normal mouse erythrocytes.

Animals↗
PubMedDate not supplied

A unique T-cell receptor complex expressed on human fetal lymphocytes displaying natural-killer-like activity.

We have recently derived a series of cloned cell lines displaying natural killer (NK) cell-like activity from normal human fetal blood (25 weeks). The lines were obtained after repeated stimulation of mononuclear cells with allogeneic Epstein-Barr virus (EBV)-transformed B lymphocytes and are interleukin-2 (IL-2) dependent. Initial characterization of the clones has been reported previously. Certain of these clones have been found to have unusual surface characteristics, namely, they are recognized by several well-defined anti-T3 antibodies, but do not react with WT31, which is thought to recognise an invariant epitope of the human (Ti-alpha beta) structure. Transcription of the genes encoding the alpha- and beta-chains of the T-cell receptor was assessed in two of these clones (F6A4 and F6C7). Ti-beta genes were found to be expressed, whereas alpha messenger RNA was not detected in Northern blot analysis. These data strongly suggest that these cells do not produce a stoichiometric T3/Ti-alpha beta receptor complex. However, experiments performed with a monoclonal antibody (anti-NKFi) developed against F6C7 cells demonstrated the existence of a unique clonotypic structure [relative molecular mass (Mr) 85,000 (85K)] which is surface-associated with T3 proteins. Furthermore, both anti-T3 and anti-NKFi were found to block cytotoxic effector function. Together, the results support the view that T3 proteins are involved in non-major histocompatibility complex (MHC)-restricted cytotoxic reactions mediated by certain circulating fetal lymphocytes which are likely to use a clonotypic structure distinct from both the 'first' (alpha beta) and the putative 'second' (gamma delta) T-cell receptor to recognize their target. The present studies were designed to characterize this structure.

Antibodies, Monoclonal↗
PubMed1989

Clonal deletion of B lymphocytes in a transgenic mouse bearing anti-MHC class I antibody genes.

B lymphocytes can be rendered specifically unresponsive to antigen by experimental manipulation in vivo and in vitro, but it remains unclear whether or not natural tolerance involves B-cell tolerance because B cells are controlled by T lymphocytes, and in their absence respond poorly to antigen (reviewed in ref. 7). In addition, autoantibody-producing cells can be found in normal mice and their formation is enhanced by B-cell mitogens such as lipopolysaccharides. We have studied B-cell tolerance in transgenic mice using genes for IgM anti-H-2k MHC class I antibody. In H-2d transgenic mice about 25-50% of the splenic B cells bear membrane immunoglobulin of this specificity, and abundant serum IgM encoded by the transgenes is produced. In contrast, H-2k x H-2d (H-2-d/k) transgenic mice lack B cells bearing the anti-H-2k idiotype and contain no detectable serum anti-H-2k antibody, suggesting that very large numbers of autospecific B cells can be controlled by clonal deletion.

Animals↗
PubMed1987

Evidence that the cytoskeleton plays a key role in cell adhesion.

A range of pharmacological agents with defined effects on cell metabolism was used to determine the metabolic requirements of three cell adhesion systems: aggregation of cells from the sponge, Ophlitaspongia tenuis; fibronectin-induced adhesion of fibroblasts to substrata and an in vitro murine thymocyte-macrophage interaction. Cell adhesion in all three systems was found to have similar metabolic requirements, implying that the mechanism of cell adhesion has been conserved through evolution. In fact, based on analysis of F-actin organization in fibroblasts, all of the pharmacological agents that inhibited cell adhesion were found to disrupt the cytoskeleton, suggesting that the cytoskeleton plays a central role in the adhesion process, presumably via redistribution of cell surface molecules. This concept was supported by the finding that the same drugs that inhibited cell adhesion inhibited anti-Ig-induced redistribution of surface Ig on B lymphocytes. The drug inhibition studies also revealed that two drugs, bromophenacyl bromide (BPB) and nordihydroguaiaretic acid (NDGA), that were previously believed to be selective inhibitors of arachidonic acid synthesis and metabolism, are also potent disruptors of the cytoskeleton.

Acetophenones↗
PubMed2002

Role of ICAM-3 in the initial interaction of T lymphocytes and APCs.

Antigen-independent adhesive interactions between T lymphocytes and antigen-presenting cells (APCs) are essential for scanning for specific antigens on the APC surface and for initiating the immune response. Here we show, through time-lapse imaging of live cells, that the intercellular adhesion molecule 3 (ICAM-3, also known as CD50) is clustered specifically at the region of the T lymphocyte surface that initiates contact with APCs. We describe the role of ICAM-3 in T cell-APC conjugate formation before antigen recognition, in early intracellular signaling and in cytoskeletal rearrangement. Our data indicate that ICAM-3 is important in the initial scanning of the APC surface by T cells and, therefore, in generating the immune response.

Adaptor Proteins, Signal Transducing↗