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Query: UNIPROT:P15088 (mast cell)
14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Peritoneal mast cells from immunized rats can form rosettes with antigen-coated sheep red blood cells. The receptor responsible for this active rosette formation is shown to be IgE cytophilic antibody: rosettes are inhibited by previous contact of mast cells with antigen, or with anti-IgE antiserum; the kinetics of mast cell rosettes following a primary immunization with ovalbumin and Bordetella pertussis vaccine is similar to the kinetics of reaginic antibody response. Furthermore, a reaginic serum can induce passive rosette formation. There is no correlation between cell-bound and circulating IgE.
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PMID:Rosette-forming mast cells in rat anaphylaxis. Immunological characteristics of mast cell rosettes. 7 5

A comparative study was carried out on the effects of a soluble derivative of baicalein, disodium baicalein 6-phosphate (BPS) and disodium cromoglycate (DSCG) on the immediate type allergic reactions. BPS not only inhibited reaginic antibody-mediated reactions including antigen-induced mediator release from monkey lung, homologous PCA in rats, and reaginic antibody-mediated degranulation of mast cell, but also non-reaginic antibody-mediated reactions such as mediator release from guinea pig lung sensitized with ovalbumin and that from human lung caused by anti-IgE. The agent, however, did not affect the mediator release from lung of rats sensitized with dinitrophynylated ascaris extract plus Bordetella pertussis. On the other hand, DSCG showed characteristic properties as an inhibitor of reaginic antibody-mediated reaction. It is thus assumed that the functional site of reaginic antibody is well fixed with DSCG at a definite distance between the two-chromone-nuclei while that of IgG is readily fixed with the two molecules of baicalein or BPS.
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PMID:A comparative study of the anti-allergic effects of disodium baicalein 6-phosphate (BPS) and disodium cromoglycate (DSCG). 40 19

Recent suggestions of a thymic origin or thymo-dependent differentiation of tissue mast cells prompted an investigation in the athymic nude (nu/nu) mouse. The outbred nu/nu examined were found to possess mast cells in at least comparable numbers to the phenotypically normal nu/+. These nu/nu were superior to nu/+ as recipient for mast cell-dependent, long latent period (IgE-type), passive cutaneous anaphylactic (PCA) reactions. A variety of studies performed, including competition with nu/+ serum, thymic restoration, quantitation of nu/+ homocytotropic antibody responses, comparison with axenic or young mice and time-course studies of skin sensitization suggested that the higher PCA titres in nu/nu skin were not entirely due to a lack of competitive inhibition of mast-cell sensitization. The nu/+ used in these studies were in fact poor IgE recipients, but were somewhat more sensitive than nu/nu to hypovolaemic shock induced by histamine and serotonin mixtures. Pretreatment with Bordetella pertussis greatly enhanced the sensitivity of nu/+, axenic, holoxenic and young normal mice to the vasoactive effects of histamine and serotonin, but was somewhat less effective in nu/nu and old mice.
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PMID:Passive cutaneous anaphylaxis and vasoactive amine challenge in nude (nu/nu) mice. A comparison with nu/+, axenic and young normal animals. 84 90

WBB6F1 mouse, a mast cell-deficient strain, was tested for active and passive cutaneous anaphylactic reactions. Active cutaneous anaphylaxis was not produced in mice which had been immunized for 1 to 2 weeks by an intraperitoneal injection of bovine serum albumin with either adjuvant, Freund's complete adjuvant or Bordetella pertussis organisms, even though circulatory IgE and IgG1 antibodies were raised. Passive cutaneous anaphylaxis (PCA) was also absent, when the mice had been sensitized with allogeneic IgE or IgG1 monoclonal antibodies. However, obvious PCA was produced when allogeneic or xenogeneic hyperimmune serum was employed. These findings indicate that mast cells are not necessarily needed for the production of PCA. Some mechanism quite different from the well-elucidated mechanism, i.e., IgE- or IgG1 antibody-triggered histamine release from mast cells, seems to be operative.
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PMID:Active and passive cutaneous anaphylaxis in WBB6F1 mouse, a mast cell-deficient strain. 236 26

The present study examines the influence of Freund's complete adjuvant (FCA) injections on sensitized PVG rats with respect to serum levels of IgE and IgG2 alpha antibodies and total IgE (all assessed by radioimmunoassays) and the capacity of serosal mast cells to release histamine on challenge in vitro with 'immunological' secretagogues (specific antigen, anti-IgE, concanavalin A) or with compound 48/80. The rats were immunized with 10 micrograms ovalbumin (OA); alum, Bordetella pertussis vaccine, or silica gel were employed as adjuvants. Treatment with FCA was performed by single intraperitoneal injections 3, 2, or 1 week(s) before or 1 or 2 weeks after sensitization. Tests were conducted 3 weeks after sensitization. The results show that the effect of FCA treatment varied reproducibly with the adjuvant employed for sensitization and with the timing of the FCA administration. FCA treatment could either increase, fail to affect, or decrease total serum IgE and OA-IgG2 alpha antibody levels as well as serosal mast cell responsiveness, whereas OA-IgE antibody responses were decreased or not affected. Moreover, serum levels of OA-IgE and OA-IgG2 alpha antibodies and total IgE were affected by FCA treatment independently of each other. Finally, serosal mast cell responsiveness to a given secretagogue could be influenced by the FCA treatment apparently independently of that to other secretagogues. A salient finding was that effects of FCA treatment on mast cell responsiveness did not necessarily conform to effects on antibody synthesis. Collectively, these data support the opinion that the mechanisms of action of the IgE-promoting adjuvants employed differ and suggest that the expression of serosal mast cell responsiveness to each examined secretagogue can be regulated separately. They also suggest that the serosal mast cell sensitizing capacity of homocytotropic antibodies may not be adequately quantified by immunochemical methods employing reagents prepared against IgE and IgG2 alpha protein.
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PMID:Modulatory effects of Freund's adjuvant treatment on mast cell histamine release and homocytotropic antibody synthesis. 241 66

High IgE responder rats were sensitized intraperitoneally with alum-adsorbed ovalbumin and Bordetella pertussis organisms. At day 0, 7, 14, 21 and 28 following sensitization the peritoneal cells were harvested and further processed for light and immunoelectron microscopical investigations using a specific anti-rat IgE immunogold sandwich method. The results obtained show that the number of peritoneal mast cells increase significantly during the course of sensitization. There is a time-dependent increase in the amount of immunogold particles on mast cell surfaces together with a shift of particle distribution towards the surface folds. Sensitized mast cells exhibit altered releasability as is indicated by slightly degranulated cells at day 21 and day 28 postsensitization. Additionally, about 25% of small lymphocytes which had entered the peritoneal cavity between day 7 and day 14 are heavily stained with the immunogold complex between day 14 and day 28 postsensitization. This is not so for macrophages (less than or equal to 0.2% positive cells) nor for eosinophils which do not show any staining activity at all despite they are present in high numbers.
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PMID:Time-course of IgE binding to rat peritoneal cells after sensitization with alum-adsorbed ovalbumin and Bordetella pertussis. 288 28

The effect of an additional adjuvant, Bordetella pertussis, on the clinical and histopathologic features of experimental autoimmune uveitis in black-hooded Lister rats was investigated. Disease was induced by a single footpad injection of purified retinal S-antigen in Freund's complete adjuvant. In those animals that did not receive B Pertussis the clinical features were those of a retinal vasculitis with disc edema, periphlebitis, and deep retinal infiltrates. In contrast, animals that received B pertussis developed lesions in the pigment epithelium and choroid. Histopathologic studies disclosed focal photoreceptor necrosis associated with mononuclear cell infiltration in both groups of animals. However, in the group that did not receive B pertussis the disease was predominantly a retinitis associated with perivascular infiltration of retinal vessels, whereas in the group that did receive B pertussis the main feature was a focal choroiditis, with superficial retinal lesions being rarely observed. Retinal photoreceptors were the target tissue in both groups of rats, but the route by which they were damaged was altered from predominantly retinal to choroidal by the addition of Bordetella pertussis as an adjuvant. This change may be ascribed to the ability of B pertussis toxin to sensitize vascular endothelium to local mast cell products, these cells being plentiful around choroidal vessels but absent in the retinal circulation.
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PMID:Differential effect of Bordetella pertussis on experimental posterior uveitis in the black-hooded Lister rat. 289 82

We have investigated the morphological effects of an intratracheal challenge with 50 micrograms ovalbumin (OA) on sensitized rat tracheas, in vivo. Female Sprague-Dawley rats were primed ten days before challenge with a single i.t. injection of 100 micrograms OA plus Bordetella pertussis (OA-BP). Two additional groups of animals served as controls: primed animals challenged with saline only and non-primed but OA-challenged animals. Sacrifices--and subsequent morphological studies--were performed prior to and 5, 15 and 60 min after challenge. At each time, the total numbers of epithelial nuclei, subepithelial mast cells (SEMC) and intraepithelial mast cells (IEMC) were scored in six non-adjacent cross sections per trachea. We found that: 1) priming with OA-BP alone did not induce any change in the tracheal mucosa with respect to morphological structure and mast cell counts; 2) no morphological change nor significant modification of the cell counts occurred at any time in tracheas from either of the control groups; 3) in contrast, a luminal heterogeneous exudate and a subepithelial oedema developed in 9 of the 15 tracheas of primed animals within 60 min of OA challenge. In those nine tracheas, the scores of intraepithelial nuclei, of IEMC and of SEMC were found to decrease significantly 15 min after challenge as compared with starting values (p less than 0.05 for each score). The decrease in the number of mucosal mast cells is probably related to the damages of the epithelial cells and to the difficulty with which depleted mast cells can be seen by toluidine blue staining.
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PMID:Morphological changes in rat tracheal mucosa immediately after antigen challenge. 289 14

The aim of the present study was to create clearly documented immediate-type allergy to food protein in the intestine of rats and to study some pathophysiological phenomena induced by challenge with the allergen. To achieve this, rats were sensitized with ovalbumin. A passive cutaneous anaphylaxis reaction to ovalbumin was negative in all controls and positive in all test animals when Bordetella pertussis was used as adjuvant. Sixty minutes after an intravenous injection of 125I-human serum albumin and 45 min after an ovalbumin challenge, given by gavage, the rats were sacrificed. The intestine was removed and sections taken for morphologic studies. The remainder was rinsed, opened, cut into measured segments, weighed, and the radioactivity was measured. Disaccharidases, alkaline phosphatase, and protein were estimated in homogenates of epithelium. Results in both control and test animals showed that radioactivity decreased as one moved distally along the intestine. However, radioactivity was significantly higher (p less than 0.01) in the intestine of test animals than in controls. Radioactivity in liver, kidney, spleen, and lungs was identical in test and control animals. There was significant reduction in levels of alkaline phosphatase (p varied from less than 0.05 to less than 0.001), maltase (p less than 0.05), and sucrase (p less than 0.05 to less than 0.01). Lactase activity in contrast was significantly raised (p less than 0.05). There was no change in intestinal morphology or in the intestinal mast cell count.
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PMID:The effect of immediate-type gastrointestinal allergic reactions on brush border enzymes and gut morphology in the rat. 392 23

Colonies of cells termed 'giant granular leucocytes' (GGL) displaying natural killer (NK) activity were generated in cell culture. The prominent feature of these cells was the formation of large cytoplasmic pool--the 'theca'--filled up with glycogen. This was demonstrated by the strong positive red staining of the theca with periodic acid Schiff reagent (PAS) which was abolished by prior treatment with amylase. Two different procedures were employed for obtaining colonies of NK-GGL. In the first, mice were injected either with killed Corynebacterium parvum or with killed Bordetella pertusis preparations and their mesenteric lymph-node cells were grown on syngeneic X-irradiated embryonic skin fibroblast monolayers. At the foci of GGL formation the fibroblasts were killed and the cleared areas thus formed were populated by adherent GGL. In the second procedure, supernates from rat or mouse spleen cultures stimulated with concanavalin A (Con A)--Interleukin-2 (IL-2)--were added to cultures of spleen and lymph-node cells prepared from either ordinary or from athymic nude mice. Richest GGL populations developed when rat IL-2 was added to cells of nude mice. Mouse IL-2 was less consistent. With nude mouse cells it stimulated, either mast cells or GGL, or both; rat IL-2 did not stimulate mast-cell differentiation in nude mouse cultures. In contrast, supernates from lymph-node cell cultures prepared from mice infected with Schistosoma mansoni. Mucosal mast cell-stimulating factor (MMSF) stimulated the formation of colonies of mast cells but not GGL. When MMSF was added as late as 23 days, colonies of young mast cells appeared and mast cells progressively increased in number. When rat IL-2 was added to such mature mast-cell cultures on the 30th day, colonies of cytolytic-GGL appeared. These observations indicate that precursors of mast cells and GGL persist in the cultures and preserve their potential to be stimulated by T-cell factors. GGL-NK cells developed on monolayers prepared from whole embryos released substance that displayed morphology and staining characteristic of mucus. Evidence gathered from in-vitro and in-vivo studies links the in-vitro GGL-NK cells to motile cells that inhabit the mucosal epithelium. Based on the observations, a hypothesis on the function of NK cytotoxicity is brought forward. It proposes the replacement of ordinary epithelial cells, which are killed during a proliferative and differentiative response of other cells at the onset of an infection course.
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PMID:Murine interleukin-2 generates glycogen-rich and mucus-secreting NK cells. 619 79


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