UMLS:C0023418 - FACTA Search

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Query: UMLS:C0023418 (leukemia)
93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Electrochemical detection of the rat basophilic leukemia (RBL-1) cells has been carried out by applying cyclic voltammetry. The detection system consists of a basal plane pyrolytic graphite electrode and a porous nitrocellulose membrane filter to trap RBL-1 cells. When the potential of the graphite electrode was run in the range of 0-1.0 V vs SCE, RBL-1 cells gave peak currents at 0.34 V vs SCE as well as 0.65 V vs SCE. There is a linear relationship between the peak current at 0.34 V vs SCE and the cell numbers of RBL-1. In the range of (0.4-2.0) X 10(5) cells. The peak current of RBL-1 cells was attributed to serotonin. When dinitrophenylated bovine serum albumin (DNP-BSA) as a model allergen was added to RBL-1 cells sensitized with anti-DNP IgE, the peak current decreased because of the degranulation of RBL-1 cells leading to serotonin release. On the other hand, RBL-1 cells sensitized with anti-DNP IgE did not respond to egg white, pollens, house dust, and milk.
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PMID:Detection of rat basophilic leukemia by cyclic voltammetry for monitoring allergic reaction. 247

The high-affinity receptor for IgE (Fc epsilon R) is the cellular trigger of the antigen-induced activation of mast cells and basophils. To examine the functional integrity of Fc epsilon R, we have adopted a protein implantation procedure whereby the purified receptor complex was coreconstituted with Sendai virus envelopes. The latter promoted fusion of the hybrid vesicles with recipient cells such as rat basophilic leukemia, RBL-2H3, thus serving as a vehicle for the receptor. The implanted Fc epsilon R was complexed with 125I-labeled mouse IgE (anti-DNP) to permit receptor quantification as well as specific triggering by DNP20BSA. Implantation in the presence of unlabeled rat IgE, which blocked the native receptors on the recipient RBL-2H3 cells, resulted in incorporation of up to 15 ng of receptor-bound IgE/10(6) cells. This was roughly equivalent in amount to 10-20% of the native receptors on such cells. The exocytosis which was triggered in the recipient cells by reagents that specifically recognized the implanted IgE reached between 15 and 50% of the maximal response. Various treatments that interfered with the activities of the viral envelopes reduced both receptor incorporation (3-5-fold) and cell degranulation (3-10-fold). These included separation of the receptor from the reconstituted envelopes, addition of serum to the incubation mixture (to inhibit vesicle-cell binding), and trypsinization of the virus (to inhibit vesicle-cell fusion). Poly(ethylene glycol) 8000 (4%) enhanced both the incorporation of the receptor and its functional responses. These treatments distinguished between real incorporation of IgE-Fc epsilon R complexes and other mechanisms of 125I-IgE association with the recipient cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Implanted IgE-Fc epsilon R complexes elicit IgE-mediated activation of RBL-2H cells. 254 Aug 3

Previous studies have shown that hydrolysis of membrane inositol phospholipids in rat basophilic leukemia (RBL-2H3) cells depended on the rate and extent of the aggregation of receptors of IgE. This response was used as an experimental probe to study the role of IgE receptors in initiating stimulatory and inhibitory processes within the cell. The response was amplified markedly by increasing the concentration of external Ca2+ from 0 to 1 mM, but the concentration required to support half-maximal response varied from less than 0.1 mM for the most potent cross-linking reagent, DNP24BSA (24 molecules of DNP attached to 1 molecule of BSA) to 0.5 mM for the least potent reagent, aggregated OVA. The dependency of phosphoinositide hydrolysis on external Ca2+ was reduced to zero once hydrolysis of inositol phospholipids was underway but secretion of histamine remained totally dependent on the presence of 0.5 to 1 mM external Ca2+. The stimulatory response persisted as long as receptors remained aggregated but it was modulated by a biochemical process, possibly the activation of protein kinase C, that targeted specifically aggregated receptors, or an associated protein. For example, when cells had become desensitized to high concentrations of one Ag, a normal response could be evoked with a second Ag. Also cells that had become desensitized could be reactivated by permeabilizing the cells. Interestingly, bell-shaped Ag dose-response curves, which were characteristic for both the phosphoinositide and secretory responses, were transformed to sigmoid-shaped curves once cells were permeabilized and dialyzed.
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PMID:Assessment of IgE-receptor function through measurement of hydrolysis of membrane inositol phospholipids. New insights on the phenomena of biphasic antigen concentration-response curves and desensitization. 283 6

Binding of antigen to IgE-receptor complexes on the surface of RBL-2H3 rat basophilic leukemia cells is the first event leading to the release of cellular serotonin, histamine, and other mediators of allergic, asthmatic, and inflammatory responses. We have used dinitrophenol-conjugated bovine serum albumin (DNP-BSA) as well as the fluorescent antigen, DNP-B-phycoerythrin, and the electron-dense antigen, DNP-BSA-gold, to investigate dynamic membrane and cytoskeletal events associated with the release of [3H]serotonin from anti-DNP-IgE-primed RBL-2H3 cells. These multivalent antigens bind rapidly to cell surface IgE-receptor complexes. Their distribution is initially uniform, but within 2 min DNP-BSA-gold is found in coated pits and is subsequently internalized. Antigen internalization occurs in the presence and absence of extracellular Ca2+. The F-actin content of the detergent-extracted cell matrices analyzed by SDS PAGE decreases during the first 10-30 s of antigen binding and then increases by 1 min to almost double the control levels. A rapid and sustained increase is also observed when total F-actin is quantified by flow cytometry after binding of rhodamine-phalloidin. The antigen-stimulated increase in F-actin coincides with (and may cause) the transformation of the cell surface from a finely microvillous to a highly folded or plicated topography. Other early membrane responses include increased cell spreading and a 2-3-fold increase in the uptake of fluorescein-dextran by fluid pinocytosis. The surface and F-actin changes show the same dependence on DNP-protein concentration as stimulated [3H]serotonin release; and both the membrane responses and the release of mediators are terminated by the addition of the non-cross-linking monovalent ligand, DNP-lysine. These data indicate that the same antigen-stimulated transduction pathway controls both the membrane/cytoskeletal and secretory events. However, the membrane and actin responses to IgE-receptor cross-linking are independent of extracellular Ca2+ and are mimicked by phorbol myristate acetate, whereas ligand-dependent mediator release depends on extracellular Ca2+ and is mimicked by the Ca2+ ionophore A23187.
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PMID:Membrane and cytoskeletal changes associated with IgE-mediated serotonin release from rat basophilic leukemia cells. 293 14

At the entry into mitosis, cells abruptly lose membrane activities such as phagocytosis, pinocytosis, and capping. The present studies test if mitotic cells also resist functional responses to cell surface ligand-receptor interactions. The IgE receptors of RBL-2H3 rat basophilic leukemia cells were labeled with anti-dinitrophenol IgE (anti-DNP-IgE) and then cross-linked with multivalent ligands (DNP-bovine serum albumin [BSA]; DNP-B-phycoerythrin; DNP-BSA-gold). IgE-receptor cross-linking modulates cell surface organization and function and releases serotonin and other mediators of allergic and asthmatic reactions from interphase cells (Pfeiffer, J. R., JC. Seagrave, B. H. Davis, G. G. Deanin, and J. M. Oliver, 1985, J. Cell Biol., 101:2145-2155). It was found that anti-DNP-IgE-receptor complexes are preserved on the cell surface throughout mitosis; they continue to bind DNP-proteins, and the resulting antigen-IgE-receptor complexes can redistribute to coated pits on the cell surface. Furthermore, there is no loss of [3H]serotonin through mitosis. Nevertheless, antigen-stimulated [3H]-serotonin release is strongly impaired in mitotic-enriched as compared with mixed interphase or G1-enriched cell populations. In addition, antigen binding transforms the surface of interphase cells from a microvillous to a plicated topography and stimulates the uptake of fluorescein isothiocyanate-conjugated dextran by fluid pinocytosis. Mitotic cells maintain a microvillous surface topography after antigen treatment, and fluid pinocytosis virtually ceases from prometaphase to telophase. Phorbol myristate acetate, a tumor promoter that activates protein kinase C, restores surface ruffling activity to mitotic cells. Thus, the mitosis-specific freezing of membrane and secretory responses is most likely due to the failure of transmembrane signaling.
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PMID:Surface functions during mitosis in rat basophilic leukemia cells. 293 15

The high affinity receptor for IgE on rat basophilic leukemia (RBL) cells mediates antigen-triggered cellular degranulation. Polyethylene glycol-induced membrane fusion methods were used to introduce exogenous IgE receptors into living RBL cells, and these were tested for normal activities. In cell-cell fusion experiments, RBL cells with fluorescein-labeled rat IgE bound to receptors and containing [5-1,2-3H(N)]hydroxytryptamine binoxalate ([3H]5HT) in their secretory granules were fused to cells with receptors occupied by rhodamine-labeled anti-dinitrophenyl mouse IgE. The fused cells showed a uniform surface distribution of both types of IgE, which could be patched independently by anti-IgE or dinitrophenylated bovine gamma globulin (DNP16BGG). [3H]5HT release could be triggered specifically by DNP16BGG. In vesicle-cell fusion experiments, plasma membrane vesicles, with receptors occupied by fluorescein- and 125I-labeled anti-DNP mouse IgE, were fused to RBL cells containing [3H]5HT. The cells showed substantial associated fluorescein fluorescence and 125I counts, and [3H]5HT release could be triggered specifically by DNP16BGG. These experiments indicate that IgE receptors can be dissociated from their natural cellular interactions and retain the ability to reassociate with another cell's components to deliver the transmembrane signal for degranulation.
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PMID:Membrane-bound IgE receptor complexes fused with rat basophilic leukemia cells mediate degranulation. 295 80

Immunogold labeling and silver enhancement techniques are widely used to determine density and distribution of cell membrane receptors by light and transmission electron microscopy. However, these techniques have not been widely used for receptor detection by scanning electron microscopy. We used antigen- or protein A-conjugated colloidal gold particles, together with silver enhancement, sequential secondary and back-scattered electron imaging (SEI and BEI), and digital image processing, to explore cell surface distribution of IgE-receptor complexes on RBL-2H3 cells, a rat leukemia line that provides a model for the study of mucosal mast cells. Cells were first incubated with a monoclonal antidinitrophenol IgE (anti-DNP-IgE) that binds with high affinity to cell surface IgE receptors. The resulting IgE-receptor complexes were cross-linked either with the multivalent antigen, DNP-BSA-gold, or with a polyclonal anti-IgE antibody. Antibody-treated cells were labeled after fixation with protein A-gold. Fixed, gold-labeled cell monolayers were silver enhanced (or not), dehydrated, critical point-dried, and coated with gold-palladium (for SEI analysis) or carbon (for combined SEI/BEI analysis). They were observed in an Hitachi S800 SEM equipped with a field emission tip and a Robinson backscattered electron detector. An image processor (MegaVision 1024XM) digitized images directly from the S800 microscope at 500-1000 line resolution. Silver enhancement significantly improves detection of gold particles in both SEI and BEI modes of SEM. On gold-palladium-coated samples, 20-nm particles are resolved by SEI after enhancement. BEI resolves 15-nm particles without enhancement and 5- or 10-nm particles are resolved by BEI on silver-enhanced, carbon-coated samples. Neither BEI nor SEI alone can yield high resolution topographical maps of receptor distribution (BEI forms images on the basis of atomic number contrast which reveals gold but not surface features). Image analysis techniques were therefore introduced to digitize, enhance, and process BEI and SEI images of the same field of view. The resulting high-contrast, high-resolution images were superimposed, yielding well-resolved maps of the distribution of antigen-IgE-receptor complexes on the surface of RBL-2H3 mast cells. The maps are stored in digital form, as required for computer-based quantitative morphometric analyses. These techniques of silver enhancement, combined BEI/SEI imaging, and digital image analysis can be applied to analyze density and distribution of any gold-labeled ligand on its target cell.
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PMID:Mapping gold-labeled IgE receptors on mast cells by scanning electron microscopy: receptor distributions revealed by silver enhancement, backscattered electron imaging, and digital image analysis. 296 20

We have examined the effect of cross-linking IgE-receptor complexes with variable receptor-receptor distances on the transmembrane signaling that leads to degranulation of rat basophilic leukemia cells. Linear polymers of the biotin-binding protein avidin were generated with bis biotin-1,12-diamidododecane, and a dinitrophenyl-biotin conjugate was bound at each end of the polymers to form a series of rigid bivalent haptens of well-defined length. The polymers were fractionated by size with nondenaturing PAGE, electro-eluted, and tested for their ability to stimulate degranulation of rat basophilic leukemia cells sensitized with anti-DNP IgE. We found that hexamers of avidin (of length greater than or equal to 240 A) were as effective in triggering degranulation as dimers (of length approximately 80 A), while the monomeric avidin antigen (of length approximately 40 A) elicited a poorer degranulation response from the cells. The mechanism by which aggregation of cell surface receptors can initiate signal transduction is discussed in light of these results.
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PMID:Cross-linking of IgE-receptor complexes by rigid bivalent antigens greater than 200 A in length triggers cellular degranulation. 297 Oct 70

The aggregation of IgE bound to rat basophilic leukaemia (RBL) cells leads to the exocytosis of mediators, the endocytosis of the antigen-aggregated mouse IgE anti-DNP, as well as the coendocytosis of some unaggregated monomeric rat IgE (IR162) and/or unbound receptors. We describe here the relative effect on endocytosis and coendocytosis of various pharmacological agents that block or enhance exocytosis. We have previously shown that, unlike exocytosis, endocytosis by RBL and normal rat mast cells was independent of extracellular calcium. We show here that the presence of calcium chelators or antagonists also had no effect on endocytosis of cross-linked IgE. However, coendocytosis of non-cross-linked IgE was partially inhibited by the elimination of extracellular calcium and the addition of calcium chelators such as EDTA or EGTA-Mg2+. Moreover, the addition of calcium antagonists such as Ni2+ and Co2+ (5 mM) to an incubation mixture containing Ca2+ (1 mM) resulted in the complete inhibition of coendocytosis without affecting endocytosis. Other inhibitors of exocytosis such as sodium azide (10-2M), quercetin (10-4M) and dibutyryl cyclic AMP (10-2 M) blocked coendocytosis completely but had no effect on endocytosis. Sodium azide (10 mM) in combination with 2-deoxyglucose (10 mM) effectively inhibited (90%) endocytosis. Cytochalasin B (10-4 M), which was shown to enhance serotonin release, had no effect on the extent of endocytosis or coendocytosis observed 20 min after the initiation of aggregation. Thus, in RBL cells, endocytosis, coendocytosis and exocytosis exhibit distinguishable sensitivities to some pharmacological drugs.
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PMID:Comparative evaluation of the effect of pharmacological agents on endocytosis and coendocytosis of IgE by rat basophilic leukaemia cells. 301 52

T cell-replacing factor (TRF) is known to play a critical role in the regulation of B cell growth and differentiation. In this study, the role of TRF in the expression of mRNA for both IgM and IgG1 class was investigated. The TRF was purified from cellfree supernatants from a T cell hybridoma, B151K12. RNA was isolated from chronic B cell leukemia (BCL1) cells, DNP-KLH-primed B cells, or normal B cells cultured with or without LPS, and LPS plus TRF or LPS plus BSF-1. The steady state level of isotype-specific mRNA was assessed by Northern blot analysis with a mu-specific or a gamma 1-specific probe. It was demonstrated that BCL1 and purified B cells cocultured with TRF expresses increased levels (twofold and fourfold, respectively) of secreted forms of mu mRNA. Purified B cells from DNP-KLH-primed mice also expressed increased levels (twofold to fourfold) of mu as well as gamma 1 mRNA for secreted form by stimulation with TRF. Total expression of mu mRNA, however, was approximately threefold higher than that of gamma 1 mRNA. The stimulation of normal B cells with LPS plus TRF induced an increase in the levels of mu mRNA and gamma 1 mRNA expression, fourfold and threefold, respectively. However, the levels of gamma 1 mRNA expression was one-third of that induced in B cells stimulated with LPS plus BSF-1. These results indicate that TRF preferentially induces increased levels of secreted type of mu mRNA and induces less gamma 1 mRNA than BSF-1. The differential role of TRF from BSF-1 in the expression of Ig mRNA will be discussed.
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PMID:Role of T cell-replacing factor (TRF) in the murine B cell differentiation: induction of increased levels of expression of secreted type IgM mRNA. 310 2

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