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Results for “Immunologic Capping”

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PubMed1984

Soluble immune response suppressor (SIRS) inhibits microtubule function in vivo and microtubule assembly in vitro.

Soluble immune response suppressor (SIRS) is a product of concanavalin A-stimulated murine T cells that, when activated or oxidized by macrophages or H2O2 (SIRSox), suppresses in vitro immune responses and inhibits cell division by normal and neoplastic cells. SIRSox is inactivated by a variety of electron donors, which suggests that SIRSox may be an oxidizing agent. Incubation of lymphocytes with SIRSox, but not with SIRS, partially reversed concanavalin A-mediated inhibition of capping of membrane immunoglobulin on B cells, and disrupted the cytoplasmic array of microtubules visualized by fluorescence microscopy. SIRSox also inhibited microtubule assembly in vitro in a concentration-dependent manner. Inactivation of SIRSox by dithiothreitol prevented SIRSox-mediated reversal of inhibition of capping and inhibition of microtubule assembly. These results reveal a pattern of SIRSox activity similar to sulfhydryl-dependent cytoskeletal disrupting agents (e.g., N-ethylmaleimide, cytochalasin A, p-benzoquinone), and suggest that SIRSox-mediated suppression of proliferation may involve interference with sulfhydryl-dependent cytoskeletal events critical for cell division.

Animals↗
PubMed1984

A kinetic study of membrane immunoglobulin capping by flow cytometry.

A flow cytometric procedure has been developed for performing kinetic studies on the capping of membrane immunoglobulin (mIg) on B lymphocytes. Mouse B cells were stained with fluorescein-conjugated antimouse-Ig antisera and subjected to pulse-shape (width, peak, and area) analyses prior to, during, and after ligand-induced redistribution of mIg. It was found that ring-stained, patched, and capped cells could be discriminated based on the width of the electronic signal curve generated as the cells passed through the laser beam. Additionally, endocytosis and or shedding of the cap could be correlated with a change in the area under the curve. Using these two parameters (width and area), the effects of temperature, cross-linking, and several pharmacological agents on the capping process were examined. Through the use of flow cytometry, the inhibitory effects of various perturbants could be localized to discrete stages of the capping process.

Animals↗
PubMed1978

Unusual antibody-induced modulation of surface antigens in the cell coat of a bloodstream trypanosome.

Unlike other eukaryotic cells, Trypanosoma lewisi forms caps at 0 degrees C when incubated with rabbit immunoglobulin G(IgG) directed against surface IgG from the rat host. The host IgG, which is specific for parasite antigens, probably does not cause capping of these antigens in vivo, since trypanosomes treated with Fab fragments directed against rat IgG are uniformly labeled and do not cap at 0 degrees C or 37 degrees C.

Animals↗
PubMed1981

Capping of surface immunoglobulin on rabbit and mouse lymphocytes. II. Cytoskeletal involvement in different subpopulations.

The role of cytoskeletal microfilaments in the cap formation of surface immunoglobulin (sIg) of rabbit spleen and peripheral blood B lymphocytes was investigated using inhibitors such as colchicine, cytochalasin B, cytochalasin D or combinations of these drugs. By immunofluorescence combined with phase contrast microscopy, analysis and sorting with a fluorescence activated cell sorter, combined staining of membrane-bound and cytoplasmic immunoglobulin, and electron microscopy, it could be established that spleen B lymphocytes consist of two subpopulations with different capping behaviour: 1. A majority of small (5-7 micrometer diameter) lymphocytes with the morphology of resting cells. This cell type was unable to form caps ("non-cappable"), and formed patches which rapidly underwent endocytosis. In these cells a connection of sIg with microfilaments is postulated, as they were triggered to cap formation in the presence of cytoskeletal inhibitors. 2. A minority of large (6-13 micrometer diameter) lymphocytes with morphological features of slightly activated cells. These cells display cap formation independent of microfilament activity. Cytoplasmic staining revealed that, although they should be considered to be rather differentiated by their age-dependent occurrence, they do not belong to the plasmablast-plasma cell series. These results demonstrate that cytoskeletal microfilaments in rabbit B cells do not play a role in generating the driving force of sIg cap formation.

Animals↗
PubMed2000

CD44 supports T cell proliferation and apoptosis by apposition of protein kinases.

T cell activation is supposed to require two signals via the TCR and a co-stimulatory molecule. However, the signaling cascade of co-stimulatory molecules has remained elusive. Here we provide evidence that CD44, which is constitutively associated with Ick and fyn, supports proliferation as well as apoptosis mainly, if not exclusively, by enhancing signal transduction via the TCR/CD3 complex. Antigenic stimulation of a T helper line in the presence of a CD44 receptor globulin was accompanied by a significant decrease in IL-2 production. To evaluate the underlying mechanism, CD44 was cross-linked via an immobilized antibody (IM-7). Cross-linking of CD44 induces proliferation of peripheral T cells and apoptosis of thymocytes and a T helper line in the presence of subthreshold levels of anti-CD3. Several proteins are rapidly tyrosine phosphorylated; erk and c-jun are strongly activated; expression of CD69 and CD25 is up-regulated on mature T cells; and expression of CD95 and CD95L is up-regulated on the T helper line. All these phenomena become less dependent of CD44 in the presence of high amounts of anti-CD3. Furthermore, cross-linking of CD44 is only effective when supporting co-localization of CD44 with the TCR/CD3 complex, since mixtures of beads coated with either anti-CD3 (low dose) or anti-CD44 do not induce T cell activation. These findings imply the rearrangement of adhesion molecules with apposition of protein kinases as a critical event for the initiation of signaling via the TCR/CD3 complex.

Animals↗
PubMed1991

The effect of heating on the expression and function of CD-2 molecules on human T-lymphocytes.

CD-2 molecules on the surface of human T-lymphocytes endow these cells with the capacity of binding sheep (SRBC) and human red blood cells (HRBC). It has recently become clear that they play an important role in the regulation of T-cell functions. The aim of the present study was to analyze the effect of heating at 45 degrees C for 1 hour on the capacity of human T-lymphocytes to bind SRBC and HRBC and to stain with CD-2 monoclonal antibody. Heating of human peripheral blood lymphocytes (PBL), thymus cells, or cells of the HD-MAR T-cell line drastically reduced their capacity of forming rosettes with SRBC. Heating of human thymus and HD-MAR cells also abrogated the formation of rosettes with HRBC. In contrast, the proportion of cells stained by high concentrations of CD-2 MoAb was reduced by only about 10-15%. Using radioiodine-labeled CD-2 MoAb, heating was found to reduce the number of cell surface E-receptors by 42% on PBL and by 27% on HD-MAR cells. The molecular weight of CD-2 molecules present on heated T-cells was identical with that of E-receptors on unheated cells. Heating was found to abolish antibody-induced capping of CD-2 molecules. Thus, heat treatment of human T-cells resulted in a moderate reduction in the number of cell-surface CD-2 molecules and in impaired mobility of CD-2 molecules in the membrane. It remains possible that in addition heating may affect the functional integrity of E-receptors or induce metabolic alterations detrimental for rosette formation.

Antibodies, Monoclonal↗
PubMed1982

Two distinct Fc receptors for IgG on human peripheral T lymphocytes.

The proportion of human peripheral T lymphocytes forming rosettes with IgG-coated ox erythrocytes (ORBC) is increased after controlled hypotonic treatment. This increment may be as high as 40% of total T cells, depending on the lymphocyte donor. Such treatment is shown not to result in selective cell loss. Induced rosetting is mediated by a receptor specific for the Fc portion of human IgG (Fc gamma R). Inhibition of induced Fc gamma R activity is equally well accomplished by monomeric and by aggregated IgG of defined size. This is in contrast to the Fc gamma R detected before hypotonic treatment, which is not significantly inhibited by monomeric IgG. Capping studies established the structural independence of these two types of Fc gamma R in the lymphocyte membrane by virtue of selective cross-linking of either receptor while leaving the respective counterpart unaffected. The biochemical basis of the hypotonic effect is not yet resolved. However, the data presented suggest that hypotonicity results in removal of Fc gamma R-bound cytophilic IgG. Operationally, we propose the term induced Fc gamma R (Fc gamma R-I) for the here-described new type of receptor with high affinity for monomeric IgG.Fc gamma R that are directly assayable without hypotonic induction and not inhibited by monomeric IgG are termed free Fc gamma R (Fc gamma R-F).

Animals↗
PubMed1988

Enhancement of lectin-induced cap formation in human neutrophils by cyclosporin A.

Cyclosporin A, a potent immunosuppressive agent, has been extensively studied for its immunomodulatory effects on T-cells. Recently Cyclosporin A has been shown to cause renal damage, which correlates with increased glomerular neutrophil migration. The precise role of Cyclosporin A on neutrophil function has not been established. In this study we investigated the role of Cyclosporin A in the regulation of cap formation in human neutrophils. Our results show an increased concanavalin A-induced cap formation in human neutrophils pretreated with Cyclosporin A, implicating a possible role of Cyclosporin A in human neutrophil activation. The correlation between enhanced capping, renal nephrotoxicity and neutrophil migration remains to be studied.

Concanavalin A↗
PubMed1982

An evaluation of lymphocyte capping in Duchenne muscular dystrophy.

There have been conflicting reports of lymphocyte capping abnormalities in Duchenne muscular dystrophy (DMD). We have evaluated the original method described by Verrill et al. in a "blind" study of 24 Duchenne muscular dystrophy boys and paired age-matched control boys. We found no differences in capping between the two groups but control boys had decreased capping compared to a group of normal adult males and females. It is concluded that the initial reports of decreased capping in DMD may have been due to differences in age between the test and control group.

Adult↗
PubMed1978

Analogous ultrastructure and surface properties during capping and phagocytosis in leukocytes.

Ultrastructural analyses have revealed striking similarities between Concanavalin A capping and phagocytosis in leukocytes. Both processes involve extensive membrane movement to form a protuberance or pseudopods; a dense network of microfilaments is recruited into both the protuberance and the pseudopods; microtubules are disassembled either generally (capping) or in the local region of the pseudopods (phagocytosis); and cells generally depleted of microtubules by colchicine show polarized phagocytosis via the microfilament-rich protuberance rather than uniform peripheral ingestion of particles via individual pseudopods. Cap formation can thus be viewed as occurring as an exaggeration of the same ultrastructural events that mediate phagocytosis. Similar changes in cell surface topography also accompany capping and phagocytosis. Thus, in nonfixed cells, Concanavalin A-receptor complexes aggregate into the region of the protuberance in colchicine-treated leukocytes (conventional capping) or into the region of pseudopod formation in phagocytizing leukocytes. In the latter case, the movement of lectin-receptor complexes occurs from membrane overlying peripheral microtubules into filament-rich pseudopods that exclude microtubules. These data provide evidence against a role for microtubules as "anchors" for lectin receptors. Rather, they indicate a preferential movement of cell surface Concanavalin A-receptor complexes towards areas of extensive (the protuberance) or localized (pseudopods) microfilament concentration. In conventional capping, Concanavalin A must be added to the colchicine-treated cells before fixation in order to demonstrate movement of receptors from a diffuse distribution into the protuberance. However, Convanavalin A receptors are enriched in the membrane associated with phagocytic particles as compared to the remaining membrane. This particle-induced redistribution of receptors is particularly prominent in colchicine-treated cells that phagocytize and are then fixed and Concanavalin A labeled; both lectin receptors and beads are concentrated over the protuberance. Thus, the final analogy between conventionally capped and phagocytic cells is that in both cases the properties of the plasma membrane in regions of microfilament concentration are modified by Concanavalin A itself (capping) or by the phagocytized particle, to limit locally the diffusion of Concanavalin A receptors.

Animals↗
PubMed1981

Localization of sulfatoxygalactosylacylalkylglycerol at the surface of rat testicular germinal cells by immunocytochemical techniques: pH dependence of a nonimmunological reaction between immunoglobulin and germinal cells.

The synthesis of sulfatoxygalactosylacylalkylglycerol (SGG) is a marker of germinal cell differentiation during spermatogenesis. Antibodies raised against this lipid have been used to visualize SGG on the surfaces of rat spermatocytes and spermatids. An ionic interaction between SGG and immunoglobulin was shown to occur at physiological pH, resulting in high fluorescence backgrounds for control cells treated with nonimmune sera. Immunofluorescence was therefore performed at alkaline pH such that this interaction was much reduced or eliminated. A method was also developed to detect surface-bound complement fixed in the presence of anti-SGG. SGG was found to be mobile within the plane of the membrane, undergoing ligand-induced "patching" and occasional "capping." However, this phenomenon was independent of temperature.

Animals↗
PubMed1983

Infection of mouse lymphoblastoid cell lines with Mycoplasma hyorhinis: complex nature of mycoplasma-host cell interactions.

Mycoplasma hyorhinis infection of lymphoid cells is a complex process. Mycoplasmas adsorb to cell surface receptors and undergo lateral redistribution on the cell membrane. This process culminates in the formation of co-caps of mycoplasmas and specific cell surface antigens. One or more of these antigens may be a M. hyorhinis receptor(s) or may bear a receptor moiety(s). We show that the cell surface antigens Thy-1.2 and Thy-1.1, and to a lesser extent H-2 and gp70, but not T200, are co-capped with M. hyorhinis on the membranes of acutely infected mouse thymic lymphoblastoid cell lines. These antigens may represent multiple receptor(s) for M. hyorhinis since there is no correlation between the expression of any individual antigen and the susceptibility of these cell lines to infection.

Adsorption↗
PubMed1980

Lymphocyte alpha-actinin. Relationship to cell membrane and co-capping with surface receptors.

Mouse spleen lymphocytes synthesize a protein which comigrates with skeletal muscle alpha-actinin on two-dimensional gel electrophoresis and is immunoprecipitated by an antibody directed against skeletal muscle alpha-actinin. Mouse lymphocyte alpha-actinin is present in membrane fractions, and is immunoprecipitated from lymphocyte detergent lysates by an antiserum made against these purified membranes. The anti-alpha-actinin activity of this antiserum is not adsorbed after incubation with fixed intact lymphocytes. Lymphocyte alpha-actinin does not bind concanavalin A and it is inaccessible to lactoperoxidase-catalyzed surface iodination. Double immunofluorescence shows that alpha-actinin moves concurrently along the cell membrane with redistributed surface immunoglobulins and Thy-1 antigen, and remains associated up to 30 min with surface aggregates of these receptors. Our results suggest that lymphocyte alpha-actinin, as defined by molecular weight and cross reactivity with the antibody against the muscle protein, (a) is associated with the cell membrane, (b) is not expressed at the cell surface, and (c) participates in the movement of surface receptors.

Actinin↗
PubMed1985

Lymphocyte mechanical response triggered by cross-linking surface receptors.

Using a recently developed method (Petersen, N. O., W. B. McConnaughey, and E. L. Elson, 1982, Proc. Natl. Acad. Sci. USA., 79:5327-5331), we have measured changes in the deformability of lymphocytes triggered by cross-linking cell surface proteins. Our study was motivated by two previously demonstrated phenomena: the redistribution ("capping") of cross-linked surface immunoglobulin (sIg) on B lymphocytes and the inhibition of capping and lateral diffusion ("anchorage modulation") of sIg by the tetravalent lectin Concanavalin A (Con A). Both capping and anchorage modulation are initiated by cross-linking cell surface proteins and both require participation of the cytoskeleton. We have shown that the resistance of lymphocytes to deformation strongly increased when sIg or Con A acceptors were cross-linked. We have measured changes in deformability in terms of an empirical "stiffness" parameter, defined as the rate at which the force of cellular compression increases with the extent of compression. For untreated cells the stiffness was approximately 0.15 mdyn/micron; for cells treated with antibodies against sIg or with Con A the stiffness increased to approximately 0.6 or 0.4 mdyn/micron, respectively. The stiffness decreased after completion of the capping of sIg. The increases in stiffness could be reversed to various extents by cytochalasin D and by colchicine. The need for cross-linking was demonstrated by the failure both of monovalent Fab' fragments of the antibodies against sIg and of succinylated Con A (a poor cross-linker) to cause an increase in stiffness. We conclude that capping and anchorage modulation involve changes in the lymphocyte cytoskeleton and possibly other cytoplasmic properties, which increase the cellular viscoelastic resistance to deformation. Similar increases in cell stiffness could be produced by exposing cells to hypertonic medium, azide ions, and to a calcium ionophore in the presence of calcium ions. These results shed new light on the capabilities of the lymphocyte cytoskeleton and its role in capping and anchorage modulation. They also demonstrate that measurements of cellular deformability can characterize changes in cytoskeletal functions initiated by signals originating at the cell surface.

Animals↗