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Results for “Immunologic Capping”

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At least 127 records · Page 7Linked to original sources
PubMed1979

Antibody-induced capping of the intracellular stage of Trypanosoma cruzi.

Intracellular-stage Trypanosoma cruzi were isolated from infected mice. The effect of specific human antibodies on the membrane surface antigens was studied in vitro, using the immunofluorescent technique. The immune serum induced the aggregation of surface antigens, forming polar caps on the amastigotes.

Animals↗
PubMed1979

Lymphocyte capping in muscular dystrophy.

We investigated lymphocyte capping in nine patients with muscular dystrophy (seven with Duchenne dystrophy and two with limb-girdle dystrophy), nine carriers, and five normal controls. No differences between the groups were observed. Thus, we have been unable to confirm a recent report that patients with muscular dystrophy, as well as carriers, have a defect in lymphocyte capping.

Animals↗
PubMed1990

Comitogenic effect of solid-phase immobilized anti-1F7 on human CD4 T cell activation via CD3 and CD2 pathways.

We have recently developed a mAb, anti-1F7, which defines a family of structures found to include the molecule recognized by anti-Ta1 (CD26). In this paper, we demonstrated that binding of 1F7 by solid-phase immobilized anti-1F7 mAb but not anti-Ta1 mAb has a comitogenic effect by inducing proliferation of human CD4+ T lymphocytes in conjunction with submitogenic doses of anti-CD3 or anti-CD2. The proliferative response induced via the CD3-1F7 or CD2-1F7 pathways is associated with the IL-2 autocrine pathway, including IL-2 production. IL-2R expression and anti-IL-2R (Tac) inhibition. Furthermore, solid-phase immobilization of anti-1F7 but not anti-Ta1 acts in conjunction with submitogenic doses of PMA to mediate a comitogenic effect in the absence of anti-CD3 or anti-CD2, leading to CD4+ T cell proliferation. PMA treatment, in the meantime, leads to enhanced expression of 1F7 on the T cell surface. Despite its functional association with both pathways of activation, however, the 1F7 structure is not comodulated with the CD3/TCR complex nor the CD2 molecule. These findings thus suggest that the CD26 Ag is involved in CD3 and CD2-induced human CD4+ T cell activation.

Antibodies, Monoclonal↗
PubMed1987

IgE receptor-mediated depolarization of rat basophilic leukemia cells measured with the fluorescent probe bis-oxonol.

Receptor-mediated changes in plasma membrane potential were recorded in rat basophilic leukemia (RBL) cells with the potential-sensitive fluorescent indicator bis-oxonol. Depolarization of the mitochondria with metabolic inhibitors was not detected by bis-oxonol, suggesting that only potential changes across the plasma membrane were being measured. The resting membrane potential of RBL cells was largely generated by the equilibrium distribution of K+ and not through electrogenic activity of the sodium pump. Depolarization was maintained as long as IgE receptors remained aggregated. We believe that at physiologic calcium concentrations a large portion of the measured potential change may be due to calcium influx across the plasma membrane. Prevention of calcium influx by lanthanum, disruption of aggregated receptors, or prior depolarization in a high K+ saline solution completely inhibited the antigen-induced depolarization. The time course of the antigen-stimulated increase in bis-oxonol fluorescence was similar, but not identical, to the antigen-stimulated rise in cytoplasmic free ionized calcium measured with fura-2. Antigen-stimulated depolarization was inhibited by removing both calcium and sodium and could be restored by the addition of either ion. Reduction of total cellular adenosine triphosphate inhibited depolarization in response to antigen stimulation.

Adenosine Triphosphate↗
PubMed1981

Inhibition of mast cell sensitization by alloantibodies.

1. Mice peritoneal mast cells previously treated with alloantibodies directed against private and public major histocompatibility antigens became partially resistant to subsequent passive sensitization with homologous IgG1-rich serum. 2. Sensitization of the mast cells was evaluated in terms of the percentage of cells that degranulated upon challenge with the specific antigen. 3. The phenomenon was immunologically specific and the responsible alloantigens were shown to be coded by the H-2K or H-2D regions.

Anaphylaxis↗
PubMed1985

A pertussis toxin-sensitive GTP-binding protein in the human neutrophil regulates multiple receptors, calcium mobilization, and lectin-induced capping.

Human neutrophils treated with pertussis toxin had decreased functional responses to several agents including zymosan-treated serum, heat-aggregated immunoglobulin, platelet-activating factor, and fMet-Leu-Phe. Responses affected include superoxide generation and release of lysozyme. The degree and type of inhibition was dependent on the individual receptor and the cellular response studied. Measurement of intracellular calcium levels with quin-2 showed that both fMet-Leu-Phe- and platelet-activating factor-mediated increases in quin-2 fluorescence were diminished as a result of pertussis toxin treatment. fMet-Leu-Phe-mediated calcium uptake was also inhibited. However, under conditions where fMet-Leu-Phe-mediated effects on cell function were completely abolished, only a partial inhibition of 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester (TMB-8) sensitive calcium uptake was observed. A study of the linked reactions of chemotaxis, capping, and shape change revealed that chemotaxis was inhibited regardless of the chemoattractant utilized (zymosan-treated serum, fMet-Leu-Phe, and platelet-activating factor) and the associated reactions of Con A capping and fMet-Leu-Phe- or Con A-mediated shape change were reduced in pertussis toxin-treated cells. Our results suggest that multiple mediators of inflammation act through a pertussis toxin-sensitive GTP-binding protein that regulates the mobilization of internal calcium as well as calcium uptake and is, in addition, a key control element of shape change, capping, and chemotaxis.

Calcium↗
PubMed1979

The participation of alpha-actinin in the capping of cell membrane components.

By means of double fluorescence staining experiments, intracellular alpha-actinin was found to accumulate under caps and patches induced in several cells by a variety of ligands. This phenomenon was demonstrated in lymphocytes and lymphoma cells treated with anti-H-2 sera; spleen lymphocytes treated with concanavalin A or anti-immunoglobulin antibodies, and VSV-infected mouse fibroblast line MC57 treated with antiserum against viral antigens. It occurred during both rapid and slow capping processes, and could be obtained by either direct or indirect ligand-induced redistribution. These observations were carried out on whole cells. For other cytoskeletal proteins such as filamin, tropomyosin and myosin, a similar accumulation under caps was not readily apparent using whole cell mounts, although earlier experiments with frozen-sectioned cells had shown such an enrichment of myosin (as well as actin). The enrichment of alpha-actinin under the clustered surface molecules was already apparent in early stages (patching) of the capping process, with or without 10 mM sodium azide present. Prolonged incubation of the cells with the different ligands resulted in endocytosis of the ligand-receptor complex. alpha-Actinin was not associated with the inernalized complex, however, suggesting that it may dissociate from the patched or capped surface structures at some stage during endocytosis.

Actinin↗
PubMed1979

Crosslinking by ligands to surface immunoglobulin triggers mobilization of intracellular 45Ca2+ in B lymphocytes.

Detailed studies of steady-state ion fluxes in murine lymphocytes were used to examine for possible ionic changes generated by surface Ig, the antigen receptor of B lymphocytes. When bound by ligands, surface Ig triggered the mobilization and release of 45Ca2+ from the cell interior by a transmembrane process requiring crosslinking of the bound receptors. This ionic event was unique for two reasons: (a) it did not occur when other common lymphocyte surface macromolecules were bound with rabbit anti-lymphocyte antibodies; and (b) it was not accompanied by a general perturbation of lymphocyte ionic properties such as a change in 42K+ fluxes nor did it depend on the presence of extracellular ions. Capping of surface Ig shares the same time sequence, dose response, requirement for crosslinking, and lack of dependence on extracellular ions. These correlations suggest that mobilization of intracellular Ca2+ may represent an early ionic signal for the contractile activation of lymphocytes that generates capping of surface Ig.

Animals↗
PubMed1979

Density of surface immunoglobulin and capping on rat B lymphocytes. I. Changes with aging.

The rate of capping and shedding of cross-linked surface immunoglobulins (SIg) was slower in old Lewis rats (greater than 24 mo) than in young Lewis rats (3-4 mo). Analysis of spleen cell populations with the fluorescence-activated cell sorter indicated that with aging there was a loss of cells with a high density of SIg. Cells with the highest density of SIg capped and shed cross-linked SIg faster than cells with a low density of SIg. The alteration in density of SIg may account for the difference in capping kinetics. Colchicine treatment increased the rate of capping of lymphocytes from young animals, but had no effect on the capping kinetics of lymphocytes from old animals.

Aging↗
PubMed1979

Lymphocyte surface and cytoplasmic changes associated with translational motility and spontaneous capping of Ig.

Murine B-lymphocytes during translatory motion undergo a series of changes with respect to their morphology and distribution of surface immunoglobulins (Ig). The sequence of events comprising these changes was followed by fluorescence microscopy and a correlated detection of surface features by scanning microscopy on exactly the same cell. A round, presumably non-motile lymphocyte exhibited a random distribution of Ig and its surface displayed evenly distributed microvilli. Formation of a ruffled edge at one pole, accompanied by a decreased fluorescence at this pole marked the initial events of lymphocyte motility. In the subsequent stages, the ruffled edge became progressively prominent and displayed a constriction at its base, while the microvilli were displaced to the opposite pole. Ig in such lymphocytes was localized at the trailing, microvilli-rich pole. Thin sections of motile lymphocytes revealed Ig, microtubules, microfilaments and coated vesicles as the characteristic features of the trailing end. These observations may have bearing on the mechanism of lymphocyte motility and spontaneous capping of Ig.

Animals↗