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Results for “Immunologic Capping”

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PubMed1981

Observation on the capping of spleen lymphocytes from scrapie infected mice after treatment with anti Ig.

Staining of lymphocytes from scrapie-infected STU mice with FITC-labelled anti-mouse Ig revealed disturbances in the capping process when compared with lymphocytes from mock-infected animals. Quantitative evaluation indicates that 10-15% of cells from scrapie-infected animals show an altered capping behaviour. These phenomena are discussed with special reference to the role of the lymphoreticular system in early scrapie agent replication.

Animals↗
PubMed1981

Capping of a phospholipid analog in the plasma membrane of lymphocytes.

Lipid vesicles were formed by ultrasonication from N-2,4,6-trinitrophenyl, 1-acyl-2-(N-4-nitrobenzo-2-oxa-1,3-diazole) aminocaproyl phosphatidylethanolamine (Tnp-NBD-PE), a fluorescent- and hapten-conjugated phospholipid analog. The vesicles, which were nonfluorescent due to self-quenching, were further characterized by gel filtration chromatography and electron microscopy. Treatment of EL-4 lymphoma cells with these vesicles at 2 degrees C resulted in immediate dequenching of fluorescence due to dilution of the fluorescent lipid in cell membranes. Control experiments showed Tnp-NBD-PE association with cells was predominantly via a lipid transfer mechanism, with little adsorption to intact vesicles. Fluorescence microscopy of the treated cells revealed bright uniform peripheral ring staining with no apparent internal fluorescence as long as the cells were maintained at 2 degrees C. Fluorescence photobleaching recovery measurements showed that the majority (approximately 80%) of the Tnp-NBD-PE was free to diffuse in the plasma membrane of the treated cells and had a diffusion coefficient of approximately 8.5 X 10(-9) cm2/sec. These observations strongly suggest that the exogenously supplied supplied lipid was diluted in the plasma membrane of the EL-4 cells and is initially free to diffuse rapidly in the plane of the membrane consistent with its proper integration in the plasma membrane bilayer. Upon incubation of washed, vesicle-treated cells at 37 degrees C, essentially all the Tnp-NBD-PE became rapidly internalized. However, warming the cells in the presence of bound Tnp antibodies prevented the internalization of the Tnp-NBD-PE and led to the formation of caps. Capping was inhibited by azide and cytochalasin B. These results are discussed in relation to various models for the redistribution of lymphocyte plasma membrane components.

Animals↗
PubMed1979

Huntington's disease: abnormality of lymphocyte capping.

Concanavalin A-induced lymphocyte capping was studied in 30 patients with Huntington's disease (HD) and 39 controls. A significant decrease in lymphocyte capping was seen in the 24 patients with HD less than 60 years of age compared to 25 age-matched controls (p less than 0.01); above age 60, differences between patients with HD and controls were not significant. These findings lend support to previous observations that generalized membrane abnormalities are present in patients with HD. Studies of HD lymphocyte capping may permit a detailed analysis of membrane function in cells that are readily obtained from living patients.

Adult↗
PubMed1988

Impaired mobility of human T lymphocyte surface molecules during inactive systemic lupus erythematosus. Relationship to a defective cAMP pathway.

The T lymphocytes of patients with active systemic lupus erythematosus (SLE) exhibit impaired capping of the surface molecules CD3, CD4, and CD8 and a defective cAMP-dependent pathway. Since the mobility of these molecules is regulated in part by cAMP, we sought to determine whether there is a specific defect(s) along the T cell cAMP pathway that contributes to the persistent capping disorder observed during inactive SLE. The data suggest that a defect may exist at the level of cAMP-dependent protein kinase activation or at a point distally. We propose that a disorder of cAMP-dependent protein kinase activity might account for the defect of capping observed in both the CD3, CD4 (helper/inducer) and CD3, CD8 (suppressor) subsets observed in SLE.

4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone↗
PubMed2004

PrPc capping in T cells promotes its association with the lipid raft proteins reggie-1 and reggie-2 and leads to signal transduction.

The cellular prion protein (PrPc) resides in lipid rafts, yet the type of raft and the physiological function of PrPc are unclear. We show here that cross-linking of PrPc with specific antibodies leads to 1) PrPc capping in Jurkat and human peripheral blood T cells; 2) to cocapping with the intracellular lipid raft proteins reggie-1 and reggie-2; 3) to signal transduction as seen by MAP kinase phosphorylation and an elevation of the intracellular Ca2+ concentration; 4) to the recruitment of Thy-1, TCR/CD3, fyn, lck and LAT into the cap along with local tyrosine phosphorylation and F-actin polymerization, and later, internalization of PrPc together with the reggies into limp-2 positive lysosomes. Thus, PrPc association with reggie rafts triggers distinct transmembrane signal transduction events in T cells that promote the focal concentration of PrPc itself by guiding activated PrPc into preformed reggie caps and then to the recruitment of important interacting signaling molecules.

Calcium Signaling↗
PubMed1981

Reduced concanavalin A capping of neonatal polymorphonuclear leukocytes (PMNs).

Neonatal polymorphonuclear leukocytes (PMNs) have previously been shown to be chemotactically deficient. To probe the mechanism(s) responsible for this deficiency, we have investigated the phenomenon of concanavalin A-induced capping in neonatal PMNs. PMNs from cord blood of 17 healthy, full-term infants and 17 normal adult volunteers were isolated by standard Ficoll-Hypaque and dextran sedimentation. After incubation with and without colchicine, the cells were reincubated with fluorescein isothiocyanate-Con A, fixed, and prepared in wet mounts. Using a fluorescence microscope, PMNs were identified, and percentage of the capped cells was counted. Upon treatment with colchicine, adult PMNs showed a significant increase in the percentage of capped cells. By contrast, the cord blood PMNs showed no significant increase in capping after colchicine treatment. The difference between percentage of PMNs showing colchicine-induced capping in adult and cord blood was highly significant (P less than 0.01; Student's t test).

Adult↗
PubMed1983

[Possibility of prenatal diagnosis of progressive muscular dystrophy: evaluation of creatine kinase activity in serum and the capping of lymphocytes].

Duchenne muscular dystrophy is a severe inherited disease. The pathogenesis is unknown. Duchenne dystrophy is characterized by a large number of membrane abnormalities, which are manifested by a leakage of muscle enzymes, such as creatine kinase (CK), and a reduction in cap formation in lymphocytes. In the present study serum CK and percentage lymphocyte capping in 8 patients with progressive muscular dystrophy, 6 with different myopathies and normal controls are investigated. Reduced antibody-induced redistribution of membrane antigens of B and T lymphocytes and high serum CK activity is found in boys with Duchenne dystrophy if compared with normal subjects and no correlation exists between the two parameters. Our data indicate that the determination of fetal serum CK activity associated with fetal lymphocyte capping may have diagnostic value in antenatal detection of Duchenne dystrophy.

Adolescent↗
PubMed1983

Human lymphocyte capping and the effect of lanthanum in Duchenne muscular dystrophy.

Capping was studied in lymphocytes obtained from controls and patients with Duchenne muscular dystrophy. Before the induction of capping by anti-Ig antibodies the cells were incubated with increasing concentrations of calcium and lanthanum. It was found that the presence or absence of extracellular calcium had no effect. Lanthanum, which blocks active calcium extrusion, altered the proportion of capping in both controls and Duchenne lymphocytes. These observations are discussed in relation to the possible involvement of free intracellular calcium in normal controls and patients with Duchenne muscular dystrophy.

Calcium↗
PubMed1988

Temperature mediated processes in teleost immunity: differential abilities of channel catfish T and B lymphocytes to cap membrane antigen.

1. The effect of both in vivo acclimation temperature and in vitro assay temperatures on channel catfish T and B lymphocyte membrane antigen (mAg) capping were investigated to determine if capping might be the temperature sensitive step involved in the low temperature immunosuppression of channel catfish T cell responses. 2. Flow cytometry was used to monitor the kinetics of capping induced by a mouse monoclonal antibody (mAb 11G3) specific for a common antigenic determinant present on channel catfish T and B cells. Results indicated that the kinetics of mAg capping were dependent on in vitro assay and in vivo acclimation temperatures and the length of time of in vivo acclimation. 3. T cells from fish appropriately acclimated to 27 degrees C cap mAg more efficiently at low assay temperatures than do B cells. 4. Activation energies were 32 and 47 kcal/mol for B and T cells, respectively, from fish acclimated to 17 degrees C for 3 weeks, but were significantly lower (14 and 22 kcal/mol, respectively) after acclimation for 5 weeks. 5. In summary, it appears that after appropriate in vivo acclimation, channel catfish T cells are better able to cap mAg at low assay temperatures than are B cells. These results suggest that mAg capping is not the low temperature sensitive step involved in T cell immunosuppression in channel catfish.

Acclimatization↗
PubMed1990

Co-capping of ras proteins with surface immunoglobulins in B lymphocytes.

Cellular ras genes encode a family of membrane-associated proteins (p21ras) that bind guanine nucleotide and possess a low intrinsic GTPase activity. The p21ras proteins are ubiquitously expressed in mammalian cells and are thought to be involved in a growth-promoting signal transduction pathway; their mode of action, however, remains unknown. The ligand-induced movement of cell-surface receptors seems to be a primary event in the transduction of several extracellular signals that control cell growth and differentiation. In B lymphocytes, surface immunoglobulin receptors crosslinked by antibody or other multivalent ligands form aggregates called patches, which then collect into a single assembly, a cap, at one pole of the cell. This process constitutes the initial signal for the activation of a B cell. Here we show by immunofluorescence microscopy that p21ras co-caps with surface immunoglobulin molecules in mouse splenic B lymphocytes. In contrast, no apparent change in the distribution of p21ras occurs during the capping of concanavalin A receptors. The redistribution of p21ras is apparent at the early stages (patching) of immunoglobulin capping and is inhibited by metabolic inhibitors and the cytoskeleton-disrupting agents colchicine and cytochalasin D. The distribution of another membrane-associated guanine nucleotide-binding regulatory protein, the Gi alpha subunit, is not affected by surface immunoglobulin capping. These findings demonstrate that p21ras can migrate in a directed manner along the plasma membrane and suggest that p21ras may be a component of the signalling pathway initiated by the capping of surface immunoglobulin in B lymphocytes.

Animals↗
PubMed1980

Surface redistribution and release of antibody-induced caps in entamoebae.

Polyspecific antibodies bound to Entamoeba induced surface redistribution of membrane components toward the uroid region. Capping of surface antigens was obtained with a single layer of antibodies in E. histolytica and E. invadens. This surface segregation progressed to a large accumulation of folded plasma membrane that extruded as a defined vesicular cap. A spontaneous release of the cap at the end of the capping process took place. These released caps contained most of the antibodies that originally bound to the whole cell surface. Two-thirds of radiolabeled antibodies bound to the surface of E. histolytica were released into the medium in 2 h. Successive capping induced by repeated exposure of E. invadens to antibodies produced conglomerates of folded surface membrane, visualized as stacked caps, in proportion to the number of antibody exposures. These results indicate the remarkable ability of Entamoeba to rapidly regenerate substantial amounts of plasma membbrane. The properties of surface redistribution, liberation of caps, and plasma membrane regeneration, may contribute to the survival of the parasite in the host during infection.

Animals↗
PubMed1982

Polymer microbeads bound to C3 fragments for detecting and labeling cells with C3 receptors.

Monodisperse microbeads (mbs) of a hydrophilic polymer with diameters of 4 microns and 0.2 micron were prepared. To these mbs, IgM or a sugar was bound covalently, and then the mbs were treated with fresh human or mouse serum. This led to the activation of complement and to the binding of C3 fragments to the mbs. C3 fragments fixed on mbs varied with the type of immobilized substance on the mbs and the incubation time of the mbs with fresh serum. Three kinds of mbs binding C3 fragments were prepared: mbs binding C3b, C3bi and C3d (C3hu-mbs); the ones binding C3bi and C3d (C3mu-mbs); and the ones binding only C3b (C3bhu-mbs). They formed rosettes with cells which had the corresponding receptor. When lymphocytes were incubated with C3hu- or C3bhu-mbs with a diameter of 0.2 micron, cap formation of each receptor was observed under a microscope. Once prepared, C3hu-, C3mu- and C3bhu-mbs were stable for more than 4 months.

Animals↗
PubMed1977

Inhibition of surface immunoglobulin centeral capping of Daudi cells and cell spreading of HeLa-S3 cells by neocarzinostatin.

The effects of an antitumor antibiotic, neocarzinostatin (NCS), on the surface immunoglobulin central capping induced by anti-immunoglobulin M antibody on Daudi cells and on the cell spreading of trypsinized HeLa-S3 cells were examined. Pretreatment of Daudi cells and HeLa-S3 cells with NCS, 5 to 30 micrograms/ml, for 4 hr inhibited cap formation and cell spreading, respectively. It was shown that there is a direct relationship between the dose and the degree of inhibition. Inhibitors of DNA synthesis such as bleomycin, mitomycin C, and 1-beta-D-arabinofuranosylcytosine showed no inhibitory effect on cap formation or cell spreading. However, known microtubule-acting agents such as colchicine and vinblastine sulfate completely inhibited both capping and cell spreading at a dose of 10 micrograms/ml. In view of the fact that 10 micorograms NCS per ml also inhibit the formation of microtubular paracrystals induced by vinblastine sulfate in HeLa-S3 cells and that other agents known to influence microtubule function such as local anesthetics and calcium ionophores also inhibit both paracrystal formation and cap formation, these new observations add further support to our hypothesis that NCS affects microtubular proteins transmembranously in vivo.

Anesthetics, Local↗
PubMed1994

Capping and receptor-mediated endocytosis of cell-bound verotoxin (Shiga-like toxin). 1: Chemical identification of an amino acid in the B subunit necessary for efficient receptor glycolipid binding and cellular internalization.

The glycolipid globotriaosylceramide (Gb3) is the plasma membrane receptor that mediates the internalization of verotoxin (VT1) into susceptible cells by capping and receptor-mediated endocytosis (RME). Internalization of fluorescein isothiocyanate-conjugated holotoxin into Daudi lymphoma cells was found to be slower than the pentameric receptor binding B subunit alone, suggesting that the A subunit may interact with the membrane to compromise the lateral mobility of the receptor bound B subunit. 3-D reconstruction of fluorescent images by confocal microscopy confirmed the complete internalization of holotoxin. VT1 internalization and cytotoxicity was inhibited by monodansyl cadavarine, which supports a role for clathrin coated pits in the RME of VT1. Biotinylation of the B subunit (in contrast to fluorescein labelling) was found to prevent toxin internalization. This effect correlated with reduced binding of Gb3 and reduced cytotoxicity in vitro. By cleavage of the B subunit at the single tryptophan residue, the reduced Gb3 binding and lack of cellular internalization was shown to be due to the biotinylation of lysine 53 in the VT1 B subunit. This residue was not labelled with fluorescein isothiocyanate in the native protein. This conclusion was confirmed by the finding that biotinylation of VT2c (which contains lys 53) prevented glycolipid receptor binding, whereas biotinylation of VT2e (in which lys 53 is substituted by ile) had no effect.

Amino Acid Sequence↗
PubMed1980

Capping and adenosine metabolism. Genetic and pharmacologic studies.

Capping of membrane Ig was studied in lymphocytes treated with agents that interfere with adenosine metabolism. Treatment of murine or human B cells with combinations of coformycin, an inhibitor of adenosine deaminase, homocysteine, and adenosine impaired Ig capping. Inhibition of capping was also produced by 3-deazaadenosine, a specific inhibitor of adenosylhomocysteine hydrolase. The inhibitors did not affect capping of the Thy-1 antigen or membrane sites reactive with antilymphocyte antibodies. Two patients with a hereditary deficiency in adenosine deaminase had impairment of Ig capping. Such an impairment was not found in lymphocytes of two other patients who had undergone successful bone marrow transplantation. It is known that the addition of a calcium ionophore results in activation of microfilament function and in disruption of Ig caps. The ionophore effect was not inhibited by the agents mentioned above. Our results suggest that the inhibition of Ig capping during aberrant adenosine metabolism may be caused by a methylation defect preceding the contracticle event that produces membrane reorganization.

Adenosine↗
PubMed1986

Capping of leukemic cells with monoclonal anti-HLA-A,B,C related to prognosis in childhood acute lymphoblastic leukemia.

Capping of leukemic cells with a monoclonal antibody against HLA A,B,C determinants was studied in 53 cases of childhood acute lymphoblastic leukemia (ALL). Determination of the percentages of capped cells after different times of incubation with anti-HLA A,B,C show that T ALL and common ALL do have quite different kinetics of HLA capping. In T ALL all cases reach levels of percentage of capped cells above 30%, in common ALL only 11 of 31 cases cap well. Dilution of the antiserum in 6 common ALL cases results in an increase of capped cells, but the original kinetics of the common ALL capping remain. ALL cases with capping curves above 30% have a worse prognosis (shorter continuous complete remission) than cases with capping curves below 30% in the total group as well as in the non-high-risk group.

Antibodies, Monoclonal↗
PubMed2001

Rafts and synapses in the spatial organization of immune cell signaling receptors.

The multichain immune recognition receptors (MIRRs), including the T cell and B cell antigen receptors and the high affinity receptor for IgE, play an important role in immune cell signaling. The MIRRs have no inherent kinase activity, but rather associate with members of the Src-family kinases to initiate signaling. Although a great deal is understood about the biochemical cascades triggered by MIRRs, the mechanism by which signaling is initiated was not known. The evidence now indicates that the Src-family kinases are concentrated in cholesterol- and sphingolipid-rich membrane microdomains, termed lipid rafts, that exclude the MIRRs. Upon ligand-induced crosslinking the MIRRs translocate into rafts where they are phosphorylated. The MIRRs subsequently form highly ordered, polarized structures termed immunological synapses that provide for prolonged signaling. An understanding of the biochemical composition of rafts and synapses and the mechanisms by which these form should lend insight into the regulation of immune cell activation.

Amino Acid Motifs↗
PubMed1989

Effects of capping on the non-ionic detergent solubility of rat thymocyte glycoproteins.

The non-ionic detergent solubility of surface antigens during capping, following their cross-linking by specific antibodies, was investigated for three rat thymocyte glycoproteins, the leucocyte-common antigen (L-CA), the leucocyte sialoglycoprotein (LSGP) and Thy-1, using a combination of immunofluorescence microscopy, covalent surface radiolabeling and quantitative analysis using a radiolabeled antibody. Prior to the addition of cross-linking antibody, both L-CA and LSGP were soluble in the non-ionic detergent Triton X-100, while Thy-1 was largely insoluble. Addition of sufficient antibody to induce capping led to a significant reduction in the solubility of L-CA and LSGP, even prior to warming to induce capping of the antigen under investigation. Subsequent capping did not increase the amount of insoluble antigen, suggesting that ligand binding, rather than the process of capping itself, is sufficient to cause this partial Triton insolubility. These results indicate the formation of an association between these liganded glycoproteins and the cell's detergent-insoluble cytoskeleton. In contrast, the Thy-1 antigen became progressively more extractable by Triton X-100 as the antigen was capped, suggesting that the insertion of the Thy-1 lipid tail into the plasma membrane was progressively more easily perturbed by the non-ionic detergent during the capping process. The reciprocal maintenance of solubility of either LSGP or L-CA during the capping of the other shows that the majority of the 180 kDa thymocyte L-CA molecules play no role in the mechanism of capping of LSGP. Furthermore, immunoprecipitates of solubilized L-CA contained no detectable amounts of the cytoskeletal protein fodrin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗