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

The susceptibility of congenitally anemic, and mast cell deficient W/Wv mice to infection with Strongyloides ratti was examined. After a primary infection, W/Wv mice showed greater and more persistent peak larval counts than did normal littermates. Worm expulsion was also slower in W/Wv mice than in +/+ mice. Furthermore, difference in susceptibility was expressed as early as 24 h after infection, suggesting not only that protective mechanisms of the gut but also of the connective tissue were defective in W/Wv mice. Reconstitution with bone marrow or spleen cells from +/+ mice was effective in restoring the protective response in W/Wv mice, whereas thymocytes or mesenteric lymph nodes had no effect. Both connective tissue and mucosal mast cells were repaired in W/Wv mice after marrow reconstitution and infection. Since relatively long incubation period was required for the expression of such reconstituting activities, bone marrow cells seem to contain precursor cells of the effector and/or regulator cells.
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PMID:Defective protective capacity of W/Wv mice against Strongyloides ratti infection and its reconstitution with bone marrow cells. 389 55

The gut mucosa contains lymphocyte-like cells, a proportion of which contain a small number of granules that resemble those of mast cells in that they contain histamine and stain metachromatically. It has been suggested that these granulated lymphocytes represent transitional forms in the differentiation of T cells into mast cells. We used monoclonal antibodies and the fluorescence-activated cell sorter to analyze the expression of Thy-1 and Lyt-2 antigens on gut intramucosal lymphocytes with particular emphasis on the granulated cells. A minority of the granulated cells (10 to 20%) expressed Thy-1 antigen at high levels equivalent to those on cortical thymocytes. A much higher proportion of the granulated cells (about 90%) expressed readily detectable levels of Lyt-2 antigen and the most prevalent phenotype of the granulated lymphocytes (60 to 70%) was Lyt-2+, Thy-1-. Two operationally specific preparations of growth factors, one maintaining the proliferation of T cells and containing T cell growth factor, and the other containing a factor stimulating the growth of persisting (P) cells that are probably mast cell progenitors, were tested on lymphocytes from the gut mucosa. By using the appropriate preparation of growth factors, both T and P cells could be grown readily from the preparation of gut intramucosal lymphocytes. Estimates of the frequency of P cell precursors among these cells indicated a minimum of one in 300 could give rise to cells resembling mast cells. Fractions of Lyt-2+ cells that were enriched in granulated cells had few detectable P cell precursors, an observation lessening the likelihood that the granulated cells were progenitors of the P cells. The precise relationship of the granulated lymphocytes (mainly Lyt-2+, Thy-1-) to T cells remains to be established.
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PMID:Intramucosal lymphocytes of the gut: Lyt-2 and thy-1 phenotype of the granulated cells and evidence for the presence of both T cells and mast cell precursors. 612 74

A patient with urticaria pigmentosa who gave a 40-year history of diarrhoea was found to have systemic mastocytosis with gut involvement. The radiological appearance of the gut in this disease, although not widely recognized, are specific and should be looked for carefully in patients with urticaria pigmentosa who complain of gastro-intestinal symptoms. Gastro-intestinal symptoms, due mainly to alterations in bowel motility or peptic ulceration, are said to occur in some 25-50% of cases of systemic mastocytosis (3, 6). These symptoms have usually been ascribed to generalized histamine release acting on the gut, although cases where mast cell infiltration of the bowel has occurred have also been reported (4, 5). In a review of the radiological features (2), increased gastric rugosity with or without evidence of peptic ulceration and nodular space-filling defects of the bowel mucosa were the most commonly found. Occasionally, diffuse thickening of the bowel wall was seen. It was concluded that these appearance were probably due to local release of vasoactive substances causing submucosal oedema following mast cell accumulation in the gut. Another result of such infiltration may be malabsorption (1).
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PMID:Forty years of diarrhoea in a patient with urticaria pigmentosa. 617 76

Mast cells constitute a heterogenous cell system. The specific type of mucosal mast cell (MMC) of the gut differs with respect to a number of properties from the classical connective tissue mast cell ( CTMC ) found in, e.g. skin, tongue and the peritoneal cavity. This report summarizes recent findings concerning turnover rates of amines and heparin in the two cell types. The elimination rate of radioactively prelabelled histamine, 5-hydroxytryptamine (5-HT) and heparin from peritoneal CTMC was compared with the elimination of radiolabelled histamine from tongue, where histamine is stored in CTMC and duodenum where it is stored in MMC. The elimination of histamine from peritoneal CTMC was slow (t 1/2 = 23 days) and did not differ significantly from that of 5-HT (t 1/2 = 25 days) and heparin (t 1/2 = 35 days) suggesting a low degree of secretory activity in the normal rat. The elimination rate of histamine from the tongue was also very slow. The specific radioactivity of histamine in duodenum was decreasing more rapidly. This was explained by a dilution of the radioactivity since the histamine content increased during the experimental period, and also by MMC death. The results are compatible with the assumption that CTMC and MMC are secretory cells, but with low activity until recruited by adequate, immunological or other stimuli.
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PMID:Turnover of histamine in mucosal and connective tissue mast cells of the rat. 673 Nov 77

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

The contributions of local and systemic factors to the regulation of mucosal mast cells and globule leukocytes have been examined in the rat. Nippostrongylus brasiliensis has been used to provide a potent immunological stimulus for mucosal mast cell hyperplasia and the roles of intestinal and extraintestinal sensitization observed by comparison of the gut mast cell responses to larval and adult worm infestations. Systemic effects of adult worm infestations have been examined in isolated Thiry-Vella loops of intestine. It is concluded that the extraintestinal phase of larval infestation is not obligatory for a gut mast cell response and that mast cell hyperplasia and globule leukocyte formation are not dependent on direct contact with the parasite or its products. The dissemination of the mast cell response and the general significance of the results are discussed.
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PMID:Local and systemic factors regulating mucosal mast cells. 686 62

Persisting (P) cells, homogeneous populations of cells that grow in vitro for prolonged periods provided a specific growth factor is present, resemble mast cells in many respects. An in vitro assay based on limit dilution was used to determine the frequency of precursors capable of giving rise to P cells. The incidences of P cell precursors per 10(6) cells in tissues of CBA mice in representative experiments were as follows: bone marrow, 291; spleen, 30; mononuclear blood cells, 11; popliteal lymph node, 0.5; and mesenteric lymph node, 18. P cell precursors appeared to be relatively undifferentiated, non-granulated cells; no cells with metachromatically staining granules were detected in the bone marrow or peripheral blood. Furthermore, mice of the Wf/Wf genotype that were grossly deficient in mast cells had the same frequencies of P cell precursors in bone marrow and spleen as their normal +/+ littermates. In many tissues in which we found P cell precursors, pluripotential hemopoietic stem cells are present. Among nonepithelial cells from the gut mucosa, however, in which there was a 10-fold higher frequency of P cell precursors than in bone marrow cells, pluripotential hemopoietic stem cells were undetectable, indicating the existence of committed P cell precursors distinct from pluripotential hemopoietic stem cells. The frequency of P cell precursors in mesenteric lymph nodes was more than 30-fold higher than in the popliteal lymph nodes, suggesting that antigenic stimulation influences their numbers. This latter notion is supported by the observation that after immunization in the footpad, the number of P cell precursors in ipsilateral popliteal lymph nodes rose about 35-fold. Immunization was also accompanied by a rise in mast cell numbers in draining popliteal nodes. This correlation between P cell precursors and the local production of mast cells was strengthened by the observation that the frequency of P cell precursors in cells from the gut mucosa of mice of Wf/Wf genotype, which are unable to mount an intestinal mastocytosis, was more than 1000-fold lower than in wild type mice. Thus, the precursors of P cells and probably of at least the T cell-dependent subset of mast cells appear to be generated in the bone marrow and seed as non-granulated cells via the blood to peripheral tissues such as spleen, lymph node, and mucosal surfaces. P cells appear to be in vitro counterparts of the mucosal subset of mast cells.
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PMID:Frequency of mast cell precursors in normal tissues determined by an in vitro assay: antigen induces parallel increases in the frequency of P cell precursors and mast cells. 686 35

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

Following infection with the intestinal nematode Nippostrongylus brasiliensis, mucosal mast cell (MMC) proliferated in the jejunum and the peak of this response was associated with a nine-fold increase in the level of mucosal mast cell protease (RMCPII) in the mucosa. At this stage the protease constituted 10%-15% of the soluble protein from gut homogenates. Concomitant immunoperoxidase studies showed that during the early proliferation of the MMC, only a proportion of the cells in lamina propria and none of the MMC within the epithelium contained detectable RMCPII. Fourteen and 20 days post infection and following a secondary challenge, staining for RMCPII in lamina propria MMC was much stronger and a few intraepithelial mast cells also contained RMCPII. With time after infection an increasing proportion of intestinal goblet cells were specifically labelled, indicating an accumulation either of RMCPII or of an antigenically similar enzyme within mucous glycoproteins. The significance of the high levels of protease in parasitized gut and of its apparent cellular distribution is discussed in relation to the protective response against the parasite.
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PMID:Quantitative analysis of mucosal mast cell protease in the intestines of Nippostrongylus-infected rats. 704 82

Highly purified populations of lymphocytes were obtained from the murine intestinal mucosa using EDTA-collagenase isolation procedures in combination with discontinuous density centrifugation. Intraepithelial lymphocytes (IEL) were separated from lamina propria lymphocytes (LPL) and, within these two populations, fractions enriched or depleted in gut granular lymphocytes (gGL) were obtained. Using these cells in cytotoxic assays, it was shown that both IEL and LPL possess natural killer (NK) activity, and this was associated with gGL. The major effector cells of gut NK activity appeared to be Thy-1.2+, Lyt-1.1-, and Lyt-2.1-. The susceptibility of gut NK cells to anti-Thy-1.2 plus complement (C) was significantly higher than that of splenic NK cells. In contrast, anti-asialo GM1 and anti-NK-1.2 plus C only slightly affected the gut NK activity. Thus, the phenotype of the gut NK cells appears to be different from the splenic one and provides further evidence for NK heterogeneity and establishes the compartmentalization of one NK subpopulation. Beige mice, deficient in splenic NK activity, also had very low gut NK activity. W/Wv mice, which lack mast cell precursors, had normal numbers of gGL and diminished, but still present, gut and splenic NK activity. This deficiency did not segregate with the genes responsible for the basic hemopoietic stem cell defect, and these results argue against a close ontogenetic relationship between IEL, gGL, and intestinal mucosal mast cells. The relevance of these observations to the cell lineage of the effector cell of gut NK activity is discussed.
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PMID:Characteristics of natural killer cells in the murine intestinal epithelium and lamina propria. 707 24


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