Clonal nature of mast-cell clusters formed in W/Wv mice after bone marrow transplantation

Kitamura, Yukihiko; Matsuda, Hiroshi; Hatanaka, Kenji

doi:10.1038/281154a0

Cited by 251 publications

(265 citation statements)

References 11 publications

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“…The ability of gp49B1 to suppress the mast cell response to activating concentrations of soluble SCF is consistent with the biologic necessity for mast cells to respond fully to the basal concentrations of SCF that mediate their development and survival in vivo [21] so as to provide intact cells that protect against bacterial infections [22][23][24][25][26]. The hyperresponsive phenotype in gp49B -/-mice was not the result of an abnormal level of endogenous SCF, because naïve gp49B -/-mice had normal numbers of mast cells not only in the ear [4], but also in the tongue, heart, lung, and small intestine (data not shown), indicating that the SCF-dependent, systemic development of mast cells is not negatively regulated by gp49B1.…”

Section: Effects Of Receptor Antagonists For Mast Cell Granule-derivesupporting

confidence: 62%

“…The cytokine stem cell factor (SCF) is mandatory for normal mast cell development; mice of the WBB6F1-Kit W /Kit W-v strain that have a dysfunctional form of the SCF receptor (c-kit) have essentially no tissue mast cells [21]. These mice are more susceptible to death when subjected to a microbial challenge such as acute septic peritonitis, but they can be protected by adoptive transfer of normal mast cells, an effect that is enhanced when mast cell development in vivo is amplified by provision of exogenous SCF [22][23][24][25][26].…”

Section: Introductionmentioning

confidence: 99%

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gp49B1 suppresses stem cell factor‐induced mast cell activation‐secretion and attendant inflammation in vivo

et al. 2003

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We report that gp49B1, a mast cell membrane receptor with two immunoreceptor tyrosinebased inhibitory motifs (ITIM), constitutively inhibits mast cell activation-secretion induced by stem cell factor (SCF), a tissue-derived cytokine that also regulates mast cell development. The intradermal injection of SCF into the ears of gp49B1 null (gp49B -/-) mice elicited 4-and 2.5-fold more degranulating mast cells and tissue swelling caused by edema, respectively, than in gp49B +/+ mice. SCF did not induce tissue swelling in mast cell-deficient mice, and the responsiveness of gp49B -/-mice to mast cell-associated amine and lipid mediators was unaltered. When gp49B +/+ and gp49B -/-mice were pretreated with antagonists of the amines, SCF-induced tissue swelling was reduced by G 90% and 60%, respectively, and it was reduced by G 90% in both genotypes when a cysteinyl leukotriene receptor antagonist was also provided. Hence, the dominant contribution of secretory granule amines to SCF-induced tissue swelling is the result of gp49B1-mediated inhibition of the production of cysteinyl leukotrienes by mast cells. Our findings also provide the first example of an ITIMbearing receptor that constitutively suppresses inflammation generated in vivo independently of the adaptive immune response by a receptor that signals through intrinsic tyrosine kinase activity rather than immunoreceptor tyrosine-based activation motifs.

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Section: Effects Of Receptor Antagonists For Mast Cell Granule-derivesupporting

confidence: 62%

Section: Introductionmentioning

confidence: 99%

gp49B1 suppresses stem cell factor‐induced mast cell activation‐secretion and attendant inflammation in vivo

et al. 2003

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“…TSLP expression in nasal epithelium requires mast cells and FccR in a mouse model of allergic rhinitis WBB6F1-+/+ mice with a mutation of c-kit are deficient for mast cells [18] and FccR-deficient mice showed no expression of FcR (FccRI, FccRIII, and FceRI) [19] because the expression of FcR requires a homodimer of the subunit FccR for surface expression and signal transduction in the mouse [20]. C57BL/6 and WBB6F1-+/+ mice challenged with OVA showed an infiltration of leukocytes in the nasal submucosa, whereas WBB6F1-W/W v mice and FccR-deficient mice challenged with OVA did not show any infiltration of leukocytes into the nasal submucosa, as previously described [21,22] (data not shown).…”

Section: Resultsmentioning

confidence: 99%

“…Female 4-6 wk C57BL/6 mice, WBB6F1-+/+, and WBB6F1-W/W v mice [18] were purchased from Japan SLC (Tokyo, Japan), FccR-chain deficient mice (C57BL/6 background) and mast celldeficient KitW-sh/W-sh mice on the C57BL/6 background were previously described [19,23,24], and were bred under specific pathogen-free conditions.…”

Section: Micementioning

confidence: 99%

Mast cell regulation of epithelial TSLP expression plays an important role in the development of allergic rhinitis

et al. 2008

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Epithelial cell-derived thymic stromal lymphopoietin (TSLP) is a master switch for asthma or atopic dermatitis by inducing a dendritic cell-mediated Th2-type allergic inflammation. Allergic rhinitis is also pathologically characterized by Th2-type allergic inflammation. This study demonstrates that mast cells regulate the epithelial TSLP expression in allergic rhinitis. TSLP expression was found to be up-regulated predominantly in the nasal epithelium in the ovalbumin (OVA)-sensitized and -nasally challenged mouse model of allergic rhinitis, which was abolished in mast cell-deficient WBB6F1-W/W v in comparison with control WBB6F1-+/+ mice. Similarly, the epithelial TSLP expression was reduced in Fc receptor c chain (FccR)-deficient mice, where the high-affinity IgE receptor (FceRI) is not expressed on mast cells, in comparison with control C57BL/6 mice. Furthermore, the administration of neutralizing TSLP antibody during the challenge phase of OVA inhibited the development of allergic rhinitis. These results suggest that the direct stimulation of epithelial cells by antigens alone may not be sufficient to induce TSLP expression in the nasal epithelium, and that mast cell regulation of epithelial TSLP expression, possibly via FceRI, plays an important role in the development of allergic rhinitis. Key words: Allergic rhinitis Á Epithelial cells Á Mast cells Á TSLP IntroductionThymic stromal lymphopoietin (TSLP) is an IL-7-like cytokine, which binds to a TSLP receptor (TSLPR) consisting of the IL-7 receptor a-chain (IL-7Ra) and a common c receptor-like chain (TSLPR-c) [1,2]. TSLP was originally identified as a factor derived from a thymic stromal cell line that could support the growth of a mouse B cell line [3]. However, recently, TSLP, derived from epithelial cells, has been shown to be capable of activating CD11c + myeloid DC to up-regulate costimulatory molecules, leading to the differentiation of CD4 + T cells into Th2 cells. Therefore, it plays a key role in the development of allergic diseases such as asthma or atopic dermatitis [1,2,4]. For instance, transgenic mice expressing TSLP in keratinocytes or in lung epithelial cells have been shown to develop atopic dermatitis-or asthma-like inflammation in the skin or the lung, respectively, while TSLPR null mice failed to develop an inflammatory lung response to inhaled antigen [5][6][7]. In humans, TSLP has been shown to be expressed by keratinocytes in atopic dermatitis and by bronchial epithelial cells in asthmatic airways [8,9].In contrast to the pro-allergic action of TSLP, regulation of TSLP expression in epithelial cells has not been fully elucidated. Previous studies suggest that TSLP expression in mouse keratinocytes is regulated by vitamin D and retinoic acid signaling [10] [17]. In addition, mast cells up-regulate the production of a variety of cytokines/chemokines in epithelial cells and fibroblasts, and induce the recruitment of basophils, T cells, and eosinophils into sites of allergic inflammation as well as their own intraepithelial accumulation....

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“…The interaction between the kinase receptor and its ligand is essential for the development of melanocytes, erythrocytes, germ cells, mast cells and interstitial cells of Cajal. [12][13][14][15][16] Gain-offunction mutations of the c-kit gene lead to stem cell factor-independent activation of intracytoplasmic signal transduction and finally tumor growth and differentiation. c-kit mutations have been found in mast cell tumors 17 and gastrointestinal stromal tumors (GISTs), 18 which are classified on the basis of About two-thirds of GISTs coexpress CD34 19,20 and/or bcl-2.…”

Section: Resultsmentioning

confidence: 99%

Cellular hamartoma resembling gastrointestinal stromal tumor: a solid tumor of the pancreas expressing c-kit (CD117)

et al. 2005

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Solid tumors of the pancreas are usually neoplastic. We report on two adult patients, each with a solid tumor of the pancreas that presented with an unusual histology and seemed to follow a benign course. The tumors, one located in the body and one in the tail, were well demarcated and composed of irregularly arranged but welldifferentiated acini and small intralobular and interlobular ducts embedded in predominantly hypocellular fibrotic tissue that contained fascicles of cytologically bland spindle cells. Islets were lacking, but immunohistochemical staining for chromogranin A and insulin revealed individual scattered insulin-producing cells distributed between acinar and ductal cells. The spindle cell component tissue showed coexpression of CD34, c-kit (CD117) and bcl-2. The follow-up (2 and 4 years) of the patients was uneventful. We propose to designate the tumors as 'cellular hamartoma resembling gastrointestinal stromal tumor.' Modern Pathology ( Keywords: pancreatic tumor; hamartoma; c-kit; CD34; bcl-2; differential diagnosis Well-demarcated tumor-like lesions in the pancreas are uncommon. They have been described under the term pseudotumor 1 or inflammatory pseudotumor. 2 Recently, we described a tumorous lesion that we termed pancreatic solid and cystic hamartoma. 3 Here we report on two further solid pancreatic tumors that have features in common with both hamartomas and gastrointestinal stromal tumors. Patients, materials and methodsThe cases were collected from the consultation files of the Department of Pathology of the University of Kiel, to which they had been submitted by the Department of Pathology in Dinslaken, Germany (case 1), and the Department of Pathology of the University of Coimbra, Portugal (case 2).In the first case, a 51-year-old man without clinical symptoms had a routine check-up, during which a mass, 3 cm in diameter, was detected by ultrasonography in the tail of the pancreas next to the splenic artery. This finding was confirmed by endosonography and CT. Laboratory tests were normal. As a result of the unclear nature of the tumor, abdominal surgery was performed with resection of the tumor.In the second case, a 54-year-old woman with slight abdominal discomfort was examined by ultrasonography, which revealed a well-demarcated tumor, 2 cm in diameter, in the body of the pancreas. A left-sided pancreatic resection was performed to remove the tumor. Both patients had an uncomplicated postoperative course and so far (2 and 4 years, respectively) have relapse-free follow-up.Representative 4 mm sections of formalin-fixed, paraffin-embedded tissue from both specimens were stained with hematoxylin and eosin (H&E) and periodic acid-Schiff. Immunohistochemical staining was performed using the standard avidinbiotin method against following antibodies: cytokeratin 8 (CAM 5

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Clonal nature of mast-cell clusters formed in W/Wv mice after bone marrow transplantation

Cited by 251 publications

References 11 publications

gp49B1 suppresses stem cell factor‐induced mast cell activation‐secretion and attendant inflammation in vivo

gp49B1 suppresses stem cell factor‐induced mast cell activation‐secretion and attendant inflammation in vivo

Mast cell regulation of epithelial TSLP expression plays an important role in the development of allergic rhinitis

Cellular hamartoma resembling gastrointestinal stromal tumor: a solid tumor of the pancreas expressing c-kit (CD117)

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