UNIPROT:P15088 - FACTA Search

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

The monoclonal antibody KP1 (CD68) was used to stain normal and neoplastic monocytes and macrophages in routinely processed, paraffin wax embedded tissue: mast cells also exhibited strong, consistent cytoplasmic immunoreactivity. Light microscopic findings were corroborated by electron microscopical and immunocytochemical findings. The predominant sites of immunoreactivity were the specific intracytoplasmic granules of the mast cells. All mast cell subtypes--that is, normal and reactive mast cells, such as those in lymph nodes exhibiting chronic non-specific lymphadenitis, and malignant or neoplastic mast cells in various types of mastocytosis--reacted with this antibody. This finding is of diagnostic importance, because mast cell proliferation could be mistaken for histiocyte proliferation. It also supports the hypothesis that mast cells derive from the bone marrow.
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PMID:Use of monoclonal antibody KP1 for identifying normal and neoplastic human mast cells. 174 May 28

Cathepsin B activity was demonstrated histochemically in unfixed cryostat sections of inflamed human gingiva using the 2-methoxy-4-naphthylamide (MNA) substrates Z-Val-Lys-Lys-Arg-MNA and Z-Ala-Arg-Arg-MNA with a post-azo-coupling technique. Enzyme localisation was confirmed by immunocytochemistry with polyclonal sheep anti-human cathepsin B. In both cases, staining was found in connective tissue fibroblasts and also in cells varying in shape from rounded to more irregular forms. The latter were present both in areas of cellular infiltration and in the oral and pocket epithelium. Examination of adjacent sections with monoclonal antibodies directed against leukocyte differentiation antigens showed that the rounded to irregular cells were CD68 positive macrophages and monocytes. The histochemical staining had the form of fine cytoplasmic particles consistent with the known lysosomal occurrence of cathepsin B. Cells stained by the post-coupling method using the tryptase substrates Z-Ala-Ala-Lys-MNA and D-Val-Leu-Arg-MNA showed a different distribution and morphology, with reaction product confined to mast cell granules. The differences between the cathepsin B and tryptase staining patterns were confirmed by differential extraction from cryostat sections with salt-free and high-salt buffers respectively. Biochemical characterisation of activities in the extracts with the 7-amino-4-trifluoromethyl coumarin (AFC) substrates Z-Val-Lys-Lys-Arg-AFC and Z-Ala-Ala-Lys-AFC and protease inhibitors confirmed the identity of the two enzymes. Selective inhibitors could also be used in histochemical incubations to distinguish between cathepsin B and tryptase staining.
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PMID:Comparative histochemical, biochemical and immunocytochemical studies of cathepsin B in human gingiva. 751 62

Twelve histochemical methods; affinity staining with avidin peroxidase, wheat germ agglutinin, and concavalin-A agglutinin; and an immunohistochemical stain with Kp1 (CD68) antibody were compared for their relative effectiveness in staining canine mast cell tumors. Stains were compared in 28 mast cell tumors and 19 histiocytomas. The effectiveness of the histochemical methods and the lectins decreased as the mast cells became less differentiated. None of the staining methods were positive on histiocytomas. Periodic acid-Schiff (PAS) gave positive results in a few cases of mast cell tumors where other histochemical stains were negative. Although avidin peroxidase and Kp1 antibody stained more mast cell tumors than any other method, they did not differ significantly from Luna's method, toluidine blue pH 0.5, toluidine blue pH 4.5, alcian blue pH 2.5, safranin O, Unna's method, and Giemsa. No stain was ideal for the diagnosis of canine mast cell tumors; however, this study suggests that the use of avidin peroxidase, Kp1 antibody, and PAS may give additional information for individual poorly differentiated tumors without substantial increase in time or cost.
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PMID:Canine mast cell tumors: a comparison of staining techniques. 753 14

The cell line HMC-1, derived from a patient with mast cell leukaemia, is the only established cell line exhibiting a phenotype similar to that of human mast cells. This paper reports on a detailed characterization of the expression of a panel of markers for various types of immature and mature haematopoietic cells in the HMC-1. We also studied the potential of HMC-1 to differentiate upon treatment with conditioned media from the human T-cell line Mo, retinoic acid or DMSO. HMC-1 was found to express several mast cell-related markers. A high expression of Kit, the receptor for stem-cell factor, was detected. The majority of the cells were stained with a MoAb against the mast cell-specific serine protease tryptase. Of particular interest was the finding that beta-tryptase mRNA, but not alpha-tryptase mRNA, was expressed in HMC-1. Using enzyme-histochemistry we were able to show that the beta-tryptase was enzymatically active, indicating that tryptase can form active homotetramers. Both heparin and chondroitin sulfate were found to be present in approximately equal amounts. HMC-1 lacked surface expression of the high-affinity IgE receptor, which was confirmed by the absence of mRNA of the alpha- and beta-chains of the IgE-receptor complex. However, a strong expression of the gamma-chain of the IgE-receptor complex was detected. A positive staining of the monocyte/macrophage marker CD68 was obtained, as well as a strong hybridization signal for the eosinophilic/basophilic-related differentiation marker the Charcot-Leyden crystal. Treatment of HMC-1 with conditioned media from the human T-cell line Mo, retinoic acid or DMSO induced only moderate changes in the surface or intracellular expression of the studied markers. The agents tested neither induced any of the monocyte/granulocyte markers examined, nor expression of the Fc epsilon RI alpha-chain.
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PMID:Phenotypic characterization of the human mast-cell line HMC-1. 819 Dec 24

To date, the diagnosis of mast cell disease (MCD) relied on routine plus histochemical stains. Its differential diagnosis, however, includes a variety of other hematopoietic and particularly B-cell lymphoid neoplasms that are best identified in paraffin sections using immunostains. To determine the paraffin-section immunoreactivity of MCD, 20 specimens from 14 patients with MCD and 1 bone marrow sample (from a patient with probable MCD) that showed equivocal metachromasia, were stained with antitryptase, CD68 (KP-1), CD20 (L26), antilysozyme, and antimyeloperoxidase antibodies. Ten hairy cell leukemias (HCLs), six lymphomas of parafollicular and/or monocytoid B-cell (MBCLs) and low-grade mucosa-associated lymphoid tissue (MALT) types, six granulocytic sarcomas, and five acute myeloid leukemias with monocytic differentiation (M4 and M5 types) were also stained. Tryptase positivity was identified in all of the MCD cases. The staining was moderate to strong in 20 of the 21 specimens, including the probable MCD case. No other neoplasms tested were tryptase positive. CD68 showed similar to even stronger staining in all of the specimens of MCD, HCL, granulocytic sarcoma, and acute myeloid leukemia (M4 and M5 types) tested and in five of the six MBCL and/or MALT-type lymphomas. Weak-to-moderate lysozyme staining seemed to be present in at least 7 of the MCD specimens, whereas there was a lack of staining for myeloperoxidase in 12 specimens, and 7 specimens were nonevaluable (1 case was not tested). Myeloperoxidase was identified in all of the granulocytic sarcomas and acute myeloid leukemias (M4 and M5 types) but not in any HCLs, MBCLs, or low-grade lymphomas of MALT type. CD20 was negative in all of the MCD and myelomonocytic neoplasms but positive in all of the HCLs, MBCLs, and low-grade B-cell lymphomas of MALT type. MCD, therefore, has a characteristic tryptase-positive, CD68-positive, and CD20-negative phenotype in paraffin sections. This distinguishes MCD from the hematopoietic and/or lymphoid disorders that it most closely resembles.
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PMID:Immunohistochemical characterization of mast cell disease in paraffin sections using tryptase, CD68, myeloperoxidase, lysozyme, and CD20 antibodies. 890 35

Chronic airways inflammation is one of the features of chronic obstructive pulmonary disease (COPD). We demonstrated previously that bronchiolar epithelium in COPD contains increased numbers of macrophages and mast cells. Transforming growth factor beta1 (TGF-beta1) may be involved in this influx because it has chemotactic activity for macrophages and mast cells. In this study, we examined expression patterns of TGF-beta1, TGF-beta receptors type I and II (TGF-betaRI and TGF-betaRII) by immunohistochemistry and mRNA in situ hybridization in peripheral lung tissue of 14 current or ex-smokers with COPD (FEV1 < 75%) and 14 without COPD (FEV1 > 84%). In both groups, TGF-beta1 and its receptors are present in airway and alveolar epithelial cells, airway and vascular smooth muscle cells, and tissue and alveolar CD68(+) cells (considered herein to be macrophages). In subjects with COPD, a semiquantitative analysis revealed approximately twofold higher levels of TGF-beta1 mRNA and protein in bronchiolar and alveolar epithelium (p < 0.02) as compared with subjects without COPD. With regard to bronchiolar epithelial cells, we found a significant correlation between TGF-beta1 mRNA and protein expression (r = 0.62; p < 0.002), and between the FEV1 of all subjects together and TGF-beta1 protein (r = -0.60; p < 0.0002) and mRNA (r = -0.67; p < 0. 002) levels. The epithelial expression of TGF-beta1 mRNA and TGF-beta1 protein correlates with the number of intraepithelial macrophages (both: r = 0.44; p < 0.03) whereas intraepithelial mast cell numbers correlate with epithelial TGF-beta1 mRNA expression. These data suggest a role for TGF-beta1 in recruiting macrophages into the airway epithelium in COPD.
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PMID:Transforming growth factor beta1 and recruitment of macrophages and mast cells in airways in chronic obstructive pulmonary disease. 984 91

Basic fibroblast growth factor (bFGF) is a potent mitogenic and chemotactic factor for endothelial cells and fibroblasts. To investigate the pathological role of bFGF in hypertrophic scar, we performed an immunohistochemical study on bFGF and bFGF receptor (bFGF-R) in hypertrophic scar (HS) including keloid, in comparison with normal scar (non-HS) and normal skin. To identify bFGF and bFGF-R positive cells, double immunostaining with antibody to mast cell (MC, tryptase) or tissue macrophage (CD68) was carried out. The expression of bFGF and bFGF-R in cultured fibroblasts from scars was also examined. In HS, many positive cells for bFGF or bFGF-R were observed between collagen bundles in addition to the positive area in normal skin. Although most of the positive cells for bFGF or bFGF-R were fibroblasts, the positive rates of bFGF in macrophages was also increased (p < 0.005). The positive rate of bFGF in MCs and the positive rates of bFGF-R in macrophages and MCs were not changed. No obvious difference was observed between non-HS and normal skin in the expression of bFGF and bFGF-R. Cultured fibroblasts from HS showed a strong nuclear staining of bFGF, but not from non-HS and normal skin. bFGF-R was equally expressed with a diffuse cytoplasmic pattern by fibroblasts from all sources. bFGF may play an important role in the pathological fibrotic process of HS in which fibroblasts are persistently activated. Cellular source of the abnormal bFGF in HS may be both fibroblasts themselves and macrophages.
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PMID:Expression of basic fibroblast growth factor and its receptor by fibroblast, macrophages and mast cells in hypertrophic scar. 1041 37

Mast cell sarcoma is a rare disease. We report an unusual case of this neoplasm arising in the ascending colon of a 32-year-old Japanese woman who presented with abdominal pain. An ulcerating mass in the colon was resected, along with enlarged mesenteric lymph nodes. Two years after surgery, the neoplasm recurred as left cervical lymphadenopathy and an intra-abdominal mass. Despite predonine and radiation therapy, the disease progressed, and the patient died. The tumor cells had abundant fine granular or clear cytoplasm, and oval, lobulated, or indented nuclei. Numerous mature eosinophils were intermingled with the tumor cells. Immunohistologic studies on paraffin sections demonstrated that the majority of the tumor cells were strongly positive for CD45RB, CD68, and mast cell tryptase. They were unreactive, however, with a broad spectrum of antibodies against myelomonocytic and lymphocytic antigens. The mast cell nature of this rare type of tumor can be best identifiable by immunostains for mast cell tryptase.
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PMID:Mast cell sarcoma with tissue eosinophilia arising in the ascending colon. 1043 Feb 80

Mast cell disease (MCD) is a rare proliferation that may be easily confused with other hematopoietic tumors. Several paraffin section antibodies immunoreact with mast cells but most are not specific. Tryptase, a specific marker of mast cells, may not be cost-effective to maintain in a laboratory because of the rarity of these lesions. This study was undertaken to assess the immunoreactivity of MCD and attempt to select a limited antibody panel for diagnosing MCD among hematopoietic tumors that morphologically mimic MCD. Immunophenotyping of cutaneous ( 10 cases) and extracutaneous (18 cases) MCD, as well as 94 other hematopoietic neoplasms, was performed on paraffin sections. All cases of MCD showed strong and diffuse positivity for CD68 and tryptase. In the vast majority of the cases, the mast cells were also positive for CD117 (27 of 28) and CD43 (25 of 27). Four cases (40%) of cutaneous MCD demonstrated a subpopulation of mast cells expressing myeloperoxidase (MPX), whereas all extracutaneous MCD were negative for MPX. Two (40%) extramedullary myeloid tumors (EMT) expressed CD43, CD68, CD 117, and MPX, but none expressed tryptase. CD43, CD68, CD117, and tryptase were expressed by 25%, 1%, 15%, and 1%, respectively, of all B-cell lymphoid neoplasms, and none expressed more than one of these four antigens. We conclude that (1) cutaneous MCDs may demonstrate a subpopulation of MPX antigen expressing tumor cells and may be confused with cutaneous involvement by myeloid leukemia if other antibodies are not used; (2) tryptase is the most specific mast cell marker among the antibodies studied; and, (3) the detection of tryptase, together with CD68, CD117, and usually CD43, is unique to MCD among hematopoietic tumors.
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PMID:Paraffin section immunophenotype of cutaneous and extracutaneous mast cell disease: comparison to other hematopoietic neoplasms. 1080 Sep 89

Dermal dendrocytes (DDs) are bone marrow-derived cells which are abundant in normal human and murine dermis, where they are closely associated with mast cells in the perivascular space. The biological role of DDs remains enigmatic. DDs express coagulation factor XIIIa and the recently described von Willebrand factor receptor, GPIb alpha, potentially indicating a function in tissue repair and haemostasis, although participation in antigen presentation is also speculated. In healing wounds and 'fibrohistiocytic' tumours, such as dermatofibromas, DDs are often associated with non-dendritic histiocytes, some of which also express factor XIIIa (FXIIIa). We have utilized human skin organ culture to examine the effects of various biological mediators on cytological characteristics of DDs. It was found that by 24 h in organ culture, immunoreactive DDs begin to lose their dendritic shape, assuming more rounded contours. This phenomenon was accentuated by mast cell degranulation; was independent of the nature of mast cell secretagogue; and could not be reproduced by recombinant tumour necrosis factor-alpha, a cytokine known to increase FXIIIa expression in DDs. Like their dendritic precursors, non-dendritic cells expressed variable FXIIIa, CD34 and CD68 and did not express CD1a or CD45. By ultrastructure, non-dendritic cells that develop in vitro resembled non-degenerating monocytes containing occasional primary lysosomes and lipid inclusions, and like DDs, expressed fibronexus-like plaques on the cell membrane. Transition of DDs from dendritic to non-dendritic cells as a consequence of specific microenvironmental influences may provide insight into the frequent concurrence of these two cytological types in fibrohistiocytic tissue reactions and neoplasia.
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PMID:Cytological alterations in dermal dendrocytes in vitro: evidence for transformation to a non-dendritic phenotype. 1088 40

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