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)

It has been suggested that Ag-specific T cell factors play a role in the early phase of cellular immune responses. Two of these factors are studied in this paper. The first factor is specific macrophage arming factor (SMAF), that binds to (arms) macrophages and renders them specifically cytotoxic against tumor cells. The second factor is involved in the induction of an early (2 h) mast cell-dependent hypersensitivity reaction, that precedes the delayed-type hypersensitivity response (mast cell arming T cell factor; MTCF). In this study we compare both factors in an allogeneic murine tumor system (C57BL (H-2b) mice sensitized against SL2 (H-2d) lymphoma cells), both factors were: 1) dependent on T lymphocytes for their production, 2) detectable in serum 2 to 3 days after immunization, and 3) MHC (H-2)-Ag specific. Immunochemical studies showed that both factors have a molecular mass between 45 and 90 kDa and bind to the mAb 14-30 (directed against specific T cell factors), but not to anti-kappa/lambda L chain antibodies. Furthermore, it was shown that SMAF produced in vitro could induce a mast cell-dependent early 2-h hypersensitivity reaction against SL2 tumor cells, and resembled in this way MTCF. We concluded that the biologic activities and immunochemical characteristics of SMAF and MTCF are similar. Both factors are produced during the early stages of the immune response and seem to play a role in the initiation of the cell-mediated immune response.
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PMID:Two specific T cell factors that initiate immune responses in murine allograft systems. A comparison of biologic functions. 265 69

The interleukin-2-dependent mouse natural killer (NK) cell line NKB61A2 concomitantly exhibits NK and natural cytotoxic (NC) activities. This was determined by the cells' ability to lyse both the NK-sensitive YAC-1 lymphoma and the NC-sensitive WEHI-164 fibrosarcoma cell lines in a 4- and 18-hour 51Cr release assay, respectively. Cell-free supernatant from NKB61A2 cells grown in culture for 48 h had substantial lytic activity against WEHI-164. The mouse mast cell line PT18-A17 and the rat basophilic leukemia cell line RBL-2H3, which both express NC activity, also produced a soluble factor during culture which lysed WEHI-164 cells. This activity was increased in the basophilic/mast cells by crossbridging the surface IgE receptors. Similar results were obtained by triggering the basophilic NC cells with the calcium ionophore ionomycin and the tumor promoter phorbol-12-myristate-13-acetate (PMA). Such triggering of NKB61A2 cells, however, did not significantly increase their NC activity. Interestingly, both ionomycin and PMA had an inhibitory effect on the NK activity of NKB61A2. Recently it has been found that tumor necrosis factor (TNF) is a major mediator of NC activity. To determine if the soluble factor responsible for the NC activity of the NK clone was related to TNF, a rabbit polyclonal antiserum to mouse TNF was tested against the cell-free culture medium of NKB61A2, PT18-A17, RBL-2H3 and murine recombinant TNF (Mu-rTNF). The lytic activity of the culture medium from all these cells and the Mu-rTNF control was abrogated by this antibody. These data suggest that the murine cell line NKB61A2 has both NK and NC activities and that the NC activity is due to a factor immunologically similar to TNF. In addition, the enhancement of NC activity in the NK cell line is apparently under control by a separate pathway, different from that in the basophilic cells.
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PMID:Natural cytotoxic activity in a cloned natural killer cell line is mediated by tumor necrosis factor. 276 50

Splenomegaly confirmed by surgery or necropsy in 100 dogs was diagnosed histologically as benign neoplasia (n = 1), primary splenic malignancy (n = 59), neoplastic metastases (n = 6), and nonneoplastic disease (n = 34). Dogs with known systemic disease, such as lymphoma and mast cell tumor, that caused splenomegaly were not included in the study. Hemangiosarcoma was the most common splenic disease (43 cases). Overall mean age of the dogs was 10.7 years, the most common breed was German Shepherd dog, and 72 of the dogs weighed more than 21 kg. Dogs with anemia, nucleated red blood cells, abnormal red blood cell morphology, or splenic rupture had a significantly greater chance of having splenic neoplasia (P less than 0.002). A multivariable logistic regression analysis found that the presence of anemia and splenic rupture in dogs with splenomegaly was up to 69% accurate in predicting presence of splenic neoplasia. After splenectomy, the median survival time of dogs with splenic neoplasia was 13 weeks. For dogs with nonneoplastic splenomegaly it was at least 36 weeks.
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PMID:Splenomegaly in dogs. Predictors of neoplasia and survival after splenectomy. 277 49

The histamine-producing cell-stimulating factor (HCSF) was first described as a lymphokine which is produced during secondary mixed leukocyte culture and which induces increased histamine synthesis by murine hematopoietic cells. It has been shown that it is different from interleukin 3 (IL 3), despite the fact that pure IL 3 expresses HCSF activity. Our results provide evidence that this factor (constitutively produced by the P388 D1 cell line) is identical with granulocyte-macrophage colony-stimulating factor (GM-CSF) i.e.: (a) physiochemical properties of HCSF and GM-CSF, such as molecular weight, isoelectric charge, hydrophobicity and behavior during affinity chromatography, are indistinguishable and both activities coelute during all biochemical purification procedures; (b) increased bone marrow cell histamine synthesis induced by P388 D1-derived HCSF is inhibited by anti-GM-CSF antiserum; (c) the GM-CSF cDNA probe hybridizes with a poly(A)+RNA from P388 D1 cells while no hybridizing signal was obtained with poly(A)+RNA from WEHI-3 and from P815 cells. On the other hand, the IL 3 cDNA probe hybridizes with a 1.0-kb poly(A)+RNA from WEHI-3 but not with those from P388 D1 and P815. Moreover, well known sources of GM-CSF, such as lung conditioned medium and semi-purified GM-CSF from phytohemagglutinin-induced supernatant of the murine T lymphoma LBRM-33-5 A4 (preparation devoid of IL 3), as well as recombinant murine GM-CSF, induce increased histamine synthesis by hematopoietic cells. All these results demonstrate that, in our culture conditions, the P388 D1 cell line spontaneously produces GM-CSF which is responsible for the P388 D1-induced HCS activity. Consequently, the latter is a property shared by the two distinct hematopoietic growth factors acting on the less committed cells, i.e. IL 3 and GM-CSF, whereas M-CSF or G-CSF are unable to induce histamine production. Interestingly, IL-4 which is known to support established mast cell line proliferation cannot induce HCS activity. In addition, none of the other cytokines tested, such as IL 1, IL 2, interferons or tumor necrosis factor can express HCS activity. This expression seems to be a specific property of IL 3 and GM-CSF.
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PMID:Histamine-producing cell-stimulating activity. A biological activity shared by interleukin 3 and granulocyte-macrophage colony-stimulating factor. 288 59

We have utilized a long-lived (Af X C57BL/6)F1 hybrid strain of mice for a variety of aging studies. In this report we have characterized the life expectancy and pattern of spontaneous deaths in 202 mice, malignant and nonmalignant lesions in 64 male mice dying spontaneously, and organ weights and lesions in 39 male mice killed at selected ages. The maximum age observed was 41.5 months. The principal causes of death were malignant lymphoma and alveologenic neoplasms, which were present in 56.3% and 45.3%, respectively, of the mice dying spontaneously. A variety of other neoplastic and non-neoplastic lesions that are not infrequently seen in older mice were observed in these mice. Neoplasms seen in these mice that are rare in other mice included disseminated mast cell tumors in two mice and gastric adenocarcinoma in one mouse. In comparing the diseases observed in this hybrid strain with those reported for the parent strains, there was an incidence of malignant lymphoma similar to the C57BL/6 parent, an incidence of alveologenic neoplasms intermediate between the parent strains, and a markedly reduced incidence of amyloidosis. This study provides a detailed background of baseline hematologic and morphologic data in a long-lived hybrid of two commonly used strains of mice.
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PMID:Life table analysis and pathologic observations in male mice of a long-lived hybrid strain (Af X C57BL/6)F1. 296 91

The bone marrow examination is useful in the diagnosis and management of patients with malignant lymphoma. Demonstration of marrow lymphoma is dependent on obtaining adequate and properly prepared tissue for examination. The incidence and pattern of marrow disease differ for the various Working Formulation classes of non-Hodgkin's lymphoma (NHL); low grade and high-grade NHL have the highest incidence of marrow involvement at diagnosis. Hodgkin's disease involves the marrow less commonly than NHL and is found in a histologic environment similar to that in lymph node biopsies. Several benign lesions, including reactive lymphoid aggregates, granulomas, immunoblastic lymphadenopathy, and mast cell disease, must be distinguished from NHL or Hodgkin's disease in some instances.
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PMID:Bone marrow in malignant lymphoma. 306 22

The spleen and lymph node are two of the most common organs involved in systemic mast cell disease (SMCD). However, SMCD infiltrates in the spleen and lymph node have a broad spectrum of morphological patterns which can make it difficult to recognize the diagnosis, especially when specimens are examined from patients in whom SMCD is not suspected. We reviewed the pathological features of 16 spleen and 23 lymph node specimens from 19 patients which represented all available material from a series of 58 Mayo Clinic patients with SMCD. The purpose of this study was to investigate the pathological manifestations of SMCD involvement in the spleen and lymph node and to address difficulties in differential diagnosis. All compartments of the spleen and lymph node were found to be affected by SMCD. SMCD lesions in the spleen were found in a paratrabecular (92%), parafollicular (69%), follicular (15%), and a diffuse red pulp (8%) distribution. In the lymph node, mast cell infiltrates affected the paracortex (88%), the parafollicular region (50%), the follicles (25%), the medullary cords (13%), and the sinuses (6%). Mast cells were frequently found in a perivascular location, and associated eosinophilia was common. Because of the broad spectrum of histological manifestations of SMCD in the spleen and lymph node, a wide range of differential diagnoses is discussed including follicular lymphoma, T-cell lymphoma, monocytoid B-cell hyperplasia and lymphoma, Kaposi's sarcoma, and Langerhans' cell granulomatosis.
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PMID:Pathology of the lymph node and spleen in systemic mast cell disease. 323 90

The present study was undertaken to elucidate whether B cell lymphoma and hybridoma cell lines can be stimulated by lipopolysaccharides (LPS) or by antibodies against immunoglobulin M (IgM) to produce granulocyte-macrophage colony-stimulating factor (GM-CSF). GM-CSF activity was assayed on the basophil/mast cell line PT-18 which is GM-CSF- and interleukin 3-dependent. Antibodies against murine recombinant GM-CSF were used to identify the colony-stimulating factor activity present in the supernatants of the stimulated B cell lines. When these cell lines were stimulated with LPS, two of five lymphoma and five of six hybridoma lines produced GM-CSF. Two cell lines, the B cell lymphoma M12.4.1 and the hybridoma TH2.2, were analyzed more extensively under serum-free conditions. In these two cell lines, the production of GM-CSF was dependent on the dose of LPS used and time of exposure. Antibodies against IgM stimulated the TH2.2 (IgM+) but not the M12.4.1 (IgM-) cells to produce GM-CSF. Northern blot analysis of the M12.4.1 and TH2.2 cells showed that mRNA of GM-CSF can be detected in LPS-stimulated but not in unstimulated cells. Our data show that transformed B cells can be stimulated to produce GM-CSF. The present data and previous studies on GM-CSF production by normal bone marrow-derived B cells suggest a possible participation of B cells in granulopoiesis.
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PMID:Induction of granulocyte-macrophage colony-stimulating factor by lipopolysaccharide and anti-immunoglobulin M-stimulated murine B cell lines. 331 10

Sixty-four patients with lymphoid lesions involving the lung were separated into three groups. In 32 patients, the predominant lymphoid cell population consisted of small, mature-appearing round lymphocytes with or without plasmacytoid features. This group, designated small lymphocytic proliferation (SLP), represents a heterogeneous group of pulmonary lymphocytic lesions including small lymphocytic lymphoma, lymphocytic interstitial pneumonia, and lymphoid hyperplasia (pseudolymphoma). Thirteen SLP patients were identified as having small lymphocytic lymphoma on the basis of monoclonality, progressive disease in other sites, or both. This group was morphologically identical to the remainder of the SLP patients, except for a higher incidence of plasmacytoid features (P = 0.003) and a greater degree of mast cell infiltration (P less than 0.05). Four of these 13 patients subsequently developed an aggressive large cell lymphoma resulting in death in three patients. The median survival for all of the SLP patients has not yet been reached. Patients in whom a monoclonal cell population could be established showed a slightly worse prognosis of borderline statistical significance (P = 0.09); however, the presence of a serum monoclonal gammopathy conveyed a significantly worse prognosis (P = 0.003). The remaining two groups of patients had various forms of malignant lymphoma other than the small lymphocytic type. One group of 12 patients, designated as having presumed primary lymphoma limited to one or both lungs (PL), had a prolonged course with a median survival of 117 months. The remaining 20 patients had disseminated lymphoma also involving lung (DL); DL patients had a shorter median survival of 33 months.
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PMID:Pulmonary lymphomas and other pulmonary lymphoid lesions. A clinicopathologic and immunologic study of 64 patients. 383 61

Surface membrane antigen(s) expressed on a mouse mast cell line (FMP1) have also been shown to occur on hemopoietic spleen colony-forming units (CFU-S) and granulocyte/macrophage colony- and erythroid burst-forming cells, using a xeno-antiserum raised against FMP1 cells. This mast cell model has been used to obtain antiserum and large quantities of antigen for the biochemical identification of CFU-S and progenitor cell antigen(s). Immunoprecipitation of FMP1 membrane antigens with the antiserum and subsequent polyacrylamide gel electrophoresis revealed the presence of five membrane proteins with molecular weights of 28,000, 32,000, 36,000, 50,000, and 70,000. Mouse B-lymphoma cell line W279 which reacted with anti-FMP1 serum was found to possess three immunoprecipitable surface proteins with molecular weights of 32,000, 50,000, and 70,000. Attempts have been made to identify the antigen(s) expressed by CFU-S and progenitors which were revealed by immunoprecipitation from the tumor lines. The three lower-molecular-weight proteins (Mr 28,000-36,000) were chosen for initial study. Membrane extracts of FMP1 cells were fractionated on Sephacryl S-200, and selective pools of these antigens were made. Antisera to these pools exhibited complement-dependent cytotoxicity to FMP1 cells, bone marrow CFU-S, granulocyte/macrophage colony-forming cells, and erythroid burst-forming units. These antisera immunoprecipitated Mr 28,000, 32,000, and 36,000 proteins from FMP1 cell membrane extracts but not the Mr 50,000 and 70,000 antigens. The W279 line has only one antigen (Mr 32,000) in the lower-molecular-weight range and is able to absorb anti-CFU-S and anti-progenitor activity, which suggests that it is this antigen which is expressed on hemopoietic cells. In addition, thymocytes react with anti-FMP1 serum, and the Mr 32,000 antigen was immunoprecipitated from thymus cell extracts. Binding studies with concanavalin A, wheat germ agglutinin, and lentil lectin indicated that the Mr 28,000-36,000 proteins were glycoproteins. The apparent molecular weights of these proteins on polyacrylamide gels were not altered by reduction and alkylation and therefore do not contain disulfide-linked subunits.
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PMID:Identification of a tumor cell-derived differentiation antigen on mouse colony-forming units in the spleen and progenitor cells. 402 83


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