Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In four different systems it was shown that murine delayed-type hypersensitivity (DTH) responses at 18-48 h were preceded by early 2-h responses. CBA mice immunized with picryl chloride, BDF1 mice immunized with oxazolone, BALB/c mice immunized with dinitrofluorobenzene, and C57BL/6 mice immunized with L5178Y lymphoma cells, and challenged with the appropriate specific antigen, all gave rise to expected 18-48 h delayed-in-time hypersensitivity reactions, but all of these responses were preceded by early hypersensitivity reactions that peaked at 2 h. These early 2-h reactions are transferable with T cells or with a T cell-derived, antigen-binding factor and are antigen-specific. The early and late components of DTH reactions are mast cell dependent since neither are elicited in mast cell deficient W/Wv or Sl/Sld mice. The T cell activity mediating the early component of DTH is demonstrable as early as 24 h after immunization, while the classical late component of DTH is not demonstrable until days 3-4. The difference in onset after immunization of the early and late components of DTH, and the different kinetics of these components in recipients of cell transfers that were challenged immediately or 24 h after transfer, led to the hypothesis that immunization for DTH leads to rapid induction in lymphoid organs of a certain population of T cells to produce an antigen-binding factor. This factor sensitizes peripheral tissues, probably mast cells, and local challenge with appropriate antigen leads to mast cell activation and release of the vasoactive amine serotonin, resulting in increased permeability of the local vasculature. This allows other circulating antigen-specific T cells, which are induced later after immunization, to enter the tissues and interact with antigen, resulting in production of chemoattractant lymphokines that recruit accessory leukocytes such as monocytes and polymorphs to enter the tissues via gaps between endothelial cells. These inflammatory cells, that are recruited to the site via two different T cell activities, constitute the characteristic infiltrate of DTH responses. Identification of an early 2-h component of DTH that is T cell- and mast cell-dependent provides evidence that the tissue-sensitizing, antigen-binding, T cell factor probably functions in vivo in the early phases of DTH responses.
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PMID:An early component of delayed-type hypersensitivity mediated by T cells and mast cells. 660 1

The mucosal lymphoid aggregates in lung and gut contain precursor cells destined to seed mucosal tissues with IgA containing cells. It is likely that both tissues also are sources of both IgE B cell precursors as well as the cells responsible for their regulation (38). Although the traffic of B cells is relatively well understood from the standpoint of IgA, the factors responsible for localization in mucosal tissue are at best unclear. Furthermore, little is known about the migration patterns of helper or suppressor cells of any kind and these may have, if derived from mucosal tissue, a preferential site of action in the mucosa. The mucosal mast cell may well be a cell of different lineage than the mast cell from the peritoneal cavity and may itself have a mucosal localization pattern. Much more work needs to be done to render some of these speculations onto a better factual base, and to harness these systems in provision of better approaches to vaccination and control of disease.
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PMID:Gut and bronchus associated lymphoid tissue: an overview. 675 73

Ultrastructural and ultracytochemical studies were performed on blood and bone marrow specimens from 18 patients with Philadelphia chromosome-positive blastic leukemia; 7 patients were in blast transformation following a typical history of chronic myelogenous leukemia and 11 patients presented with "acute leukemia." The patients were divided into 2 morphologic groups on the basis of light microscopic and cytochemical observations. In group I, which consisted of 11 patients, the proliferating cells were "lymphoid" in appearance and demonstrated many cytochemical, biochemical, and immunologic features similar to those of the lymphoblasts of non-T, non-B acute lymphoblastic leukemia. In group II, which consisted of 7 patients, the proliferating cells were myeloid in appearance. On the basis of ultrastructural observations, the 11 group I patients were divided into 2 subgroups, A and B. Subgroup IA, consisting of 5 patients, was characterized by blasts that demonstrated no differentiating features. In subgroup IB, consisting of 6 patients, 20-30% of the leukemic cells contained inclusions that resembled leukemic mast cell or basophil granules. The leukemic cells in the 7 group II patients manifested myeloid characteristics by light microscopy and prominent basophil and mast cell granulopoiesis by electron microscopy. Abnormalities of other myeloid cell lines were also observed in both the lymphoid and myeloid groups of patients.
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PMID:Ultrastructural features of basophil and mast cell granulopoiesis in blastic phase Philadelphia chromosome-positive leukemia. 693 33

Synthesis of specific homocytotropic antibody by cells from various lymphoid and haemopoietic organs in rats infested with Nippostrongylus brasiliensis has been studied by use of homologous adoptive cutaneous anaphylaxis and compared with the kinetics of appearance in the serum and thoracic duct lymph of specific IgE antibodies. Using this technique, synthesis of specific mast cell-sensitizing antibody has been detected in the draining lymph nodes of the lung as early as 12 days after infestation and by 14 days in the draining lymph nodes of the small intestine. Specific IgE antibody was not detected in serum until between 16 and 18 days after infestation. The delay in detection of antibody in the serum is at least in part due to its rapid removal from the blood, because antibody en route to the bloodstream from the gut-associated lymphoid tissue was detected in the thoracic duct lymph plasma as early as day 12. A major traffic of homocytotropic antibody-secreting cells has been detected in the thoracic duct lymph of the infested rats. The results are discussed in terms of the possible role of immediate hypersensitivity in the expulsion of the parasite, the origin of the IgE antibody response to the parasite and the mechanism of the potentiated reagin response.
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PMID:The distribution and traffic of specific homocytotropic antibody-synthesizing cells in Nippostrongylus brasiliensis-infested rats. Comparison of synthesis with the kinetics of antibody and IgE levels in serum and lymph. 697 8

The anaphylactic function of IgE has been intensively investigated. The Fc epsilon receptor on mast cells or basophils combines with the last two constant domains of the epsilon heavy chain. The Fc epsilon receptor is apparently a glycoprotein, monovalent and free in the plasma membrane. The interaction between the antigen (allergen) and the corresponding IgE antibody combined with the Fc epsilon receptor results in the aggregation of the receptors. Receptor dimerization suffices to trigger the cell. Compartments can be described in mast cells or basophils, the activity of which depends upon the number of formed receptor dimers on the corresponding membrane area. Beyond a threshold number of dimerized receptors, the cell compartment is triggered, which in the presence of Ca++ leads to the discharge of mast cell mediators, an increasing function of the dimer number. Excess receptor aggregation or the absence of aggregation (i.e. IgE-Ag2 complexes) deactivates the cell, which occurs more often in the absence of Ca++. Thus, IgE molecules play a passive role only in allowing the aggregation of the receptors which delivers the activating signal. But through the composition of IgE-antigen complexes bound to the receptors, IgE also modulates the cell function according two antagonistic reactions in permanent balance, i.e. activation or deactivation. IgE molecules are also involved in immediate type reactions in inducing the release of lysosomal enzymes from mononuclear phagocytes. But IgE antibody can also, when complexed with the antigen, trigger macrophage cytotoxicity for the corresponding target, which indicates a new function of IgE in the effector mechanisms of immunity of particular importance in immunity to schistosomes. A receptor for aggregated IgE has been characterized on the membrane of macrophages. The binding of IgE to its macrophage receptor triggers the cell, as shown by the resulting increase in cyclic GMP, calcium uptake and accelerated turn-over of lysosomal enzymes. A receptor for IgE has also been described on lymphoid cells, B cells, null cells and recently T cells, and the appearance of the receptor is modulated by IgE molecules themselves, suggesting a homeostatic role of IgE molecules. IgE appears thus to play various functions, the most dramatic being the triggering of anaphylactic reactions. But the role of IgE in activating mononuclear phagocytes or lymphoid cells might also prove to be of importance in immunity.
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PMID:[Cellular interactions of IgE: towards a new function for IgE]. 700 8

Clonal mast cell differentiation occurs when mesenteric lymph node cells from mice immunized with an antigen are grown in its presence on fibroblast monolayers prepared from mouse embryonic skin. Two types of mast cell clones are identified: the first, originates from a precursor present in the lymphoid cell suspension and the second, from a precursor in the fibroblast monolayer. Clones of the first type fail to appear when T cells are eliminated from the suspension; but they grow luxuriantly in the presence of fluid, harvested from cultures containing the antigen-sensitive T cells exposed to the antigen. The two mast cells differ in the clonal size and rate of growth, life span, cell size, shape and size of the granules and numbers of IgE receptors. It is concluded that the rapidly multiplying lymphoid mast cells associate with the mucosae of the respiratory and gastrointestinal tracts and appear in large number in response to immunological stimuli; the long lived mast cells derived from the embryonic skin monolayer are found in the general connective tissue.
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PMID:Mast cell growth on fibroblast monolayers: two-cell entities. 706 Nov 2

Information from the NCTR control pathology data base was examined to morphologically classify and correlate the incidence off hyperplastic and neoplastic hematopoietic lesions with age in over 15,000 male and female mice of a variety of strains. Hyperplasia affected lymphoid and reticular cells, erythropoietic and granulopoietic cells, mast cells, plasma cells and megakaryocytes. Neoplastic lesions included lymphocytic lymphoma, mixed cell lymphoma, histiocytic lymphoma, granulocytic leukemia, plasma cell neoplasms and mast cell neoplasms. Most hyperplastic and neoplastic hematopoietic lesions increased wtih age and most were slightly more common in the female than in the male mice.
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PMID:Morphologic classification and correlation of incidence of hyperplastic and neoplastic hematopoietic lesions in mice with age. 726 36

In animals with hereditary muscular dystrophy there are thymic abnormalities which may be of etiological significance in the dystrophic process. This study investigated mast cell number and histamine levels in the thymus of normal and dystrophic chickens. For comparison, other lymphoid tissues, namely the spleen and the bursa of Fabricius, and non-lymphoid tissues including the comb and pectoralis major muscle, were similarly studied. Our results show that the thymus of dystrophic adult birds has a deficiency in both mast cell number and histamine content. In the bursa of Fabricius of dystrophic birds a significant elevation in histamine content (microgram/g) was attributed to the abnormally small size of this organ, rather than to an absolute mast cell increase. The deficiency in thymic mast cell number in dystrophic chickens may be significant in the postulated abnormal thymus-muscle interaction of the dystrophic process.
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PMID:Thymic mast cell deficiency in avian muscular dystrophy. 732 98

Kimura's disease (KD) typically presents as large subcutaneous masses in young Oriental males. It is characterized by deep inflammation with vascular proliferation, lymphocytic nodules with subcutaneous germinal centers, fibrosis, and edema. In comparison, angiolymphoid hyperplasia with eosinophilia (AHLE) occurs in all races and the lesions usually are smaller and more superficial. The causes of these two diseases are debated. We compared histologic features of 4 cases of KD with 22 cases of ALHE and studied expression of endothelial antigens and lymphocyte markers as well as localization of eosinophil, mast cell, and neutrophil granule proteins in lesional tissue. T-cell lymphoid aggregates with well-formed B-cell germinal centers occurred in KD, and nodular and diffuse T-cell infiltration with small B-cell clusters occurred in ALHE. Endothelial proliferation was more pronounced in KD, lacking the atypical histiocytoid endothelial cells characteristic of ALHE. Many intact eosinophils infiltrated lesions in both diseases, although KD had less extracellular granule protein deposition than ALHE. Intact mast cells were seen in both diseases. There was neutrophil elastase staining of occasional scattered intact cells but no extracellular deposition. Compared with KD, ALHE is more varied in its clinical, histopathologic, and immunohistochemical features.
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PMID:Kimura's disease and angiolymphoid hyperplasia with eosinophilia: new observations from immunohistochemical studies of lymphocyte markers, endothelial antigens, and granulocyte proteins. 749 71

The c-kit receptor is a tyrosine-kinase transmembrane receptor first identified as an oncogene in the HZ4-feline leukemia virus and later found to be important in hematopoiesis in mice. The ligand for this receptor (Steel factor) can stimulate hematopoiesis both in vitro and in vivo. To study the pattern of c-kit receptor expression in normal human hematopoietic progenitor cells, we prepared a monoclonal antibody (9B9) against human c-kit receptor by using a synthetic peptide (amino acids 476-501) from the extracellular domain of c-kit receptor to immunize Balb/c mice. Monoclonal antibody 9B9 bound to recombinant c-kit protein, the erythroleukemic line HEL, the megakaryocytic line MEG-01, and the murine mast cell line P815. Monoclonal antibody 9B9 also bound to the surface of the CD7+CD3-CD4-CD8- T cell lymphoid cell lines DU.528 and HSB2T, and also to 1 to 4% of normal bone-marrow cells. The majority (67 +/- 6%) of CD34+ bone-marrow progenitor cells coexpressed c-kit receptor. Flow-cytometry analysis of immature CD3-CD4-CD8- (triple-negative) thymocytes indicated 30 +/- 9.5% expressed the c-kit receptor, and thymidine incorporation assay revealed that the receptor is functional. Indirect fluorescent microscopy of human thymic tissue, using a monoclonal antibody against Steel factor, revealed its presence on scattered mononuclear cells within the intralobular septae and the subcapsular cortex, which are regions where the triple-negative thymocytes are also localized. These data provide evidence that the c-kit receptor is present on human hematopoietic bone marrow and intrathymic T cell progenitor cells, and that it likely plays a role in early T cell lymphopoiesis.
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PMID:The c-kit proto-oncogene receptor is expressed on a subset of human CD3-CD4-CD8- (triple-negative) thymocytes. 752 82


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