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 this study the expression of 'classically' considered lymphoid-associated antigens (CD2, CD3, CD4, CD5, CD7, CD8, CD10, CD19, CD20, and CD22) was explored both in peripheral blood (PB) and bone marrow (BM) mast cells (MC) in a case of systemic mast cell disease (SMCD) by means of using multiple stainings and a direct immunofluorescence technique. CD2 and CD22 were expressed in both PB and BM MC, all the remaining lymphoid-associated markers were negative. Our results suggest that the reactivity for both CD2 and CD22 in PB and BM MC would be aberrant.
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PMID:Expression of lymphoid-associated antigens in mast cells: report of a case of systemic mast cell disease. 854 46

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

IL-4 is central to the formation of IgE and the development of Th2 effector cells, both key features of an allergic response. We have examined IL-4 production early in the formation of an allergic response by using a previously established human in vivo model of allergic rhinitis where allergic subjects are challenged internasally with allergen and the particulate pollutant diesel exhaust particles (DEP). This model is characterized by enhanced IgE production and deviation to a Th2-type cytokine profile in nasal lavage fluid from these subjects. In this model, IL-4 protein and IL-4-positive cells could first be detected 4 h after challenge and maximal production was observed after 18 h. Two-color flow cytometric analysis for the detection of intracellular IL-4 and surface markers was performed on nasal cells recovered 4 h after challenge. At this time, CD117(+) (c-kit+) cells constituted between 65 and 100% of the IL-4(+) cells, while 0-12% of the IL-4(+) cells were CD3 positive. No IL-4(+) CD19/CD20(+) or IL-4(+) CD56(+) cells were detected at 4 h. As the allergic response progressed the primary source of IL-4 changed. At the peak of IL-4 production, 18 h after challenge, CD3(+) comprised the majority of cells staining for intracellular IL-4 (73 to 100%). Thus we show an initial role for cells of the mast cell/basophil lineage residing in the nasal mucosa in the initial production of IL-4, which frames the subsequent immune response by expanding the repertoire of TH2 cytokine-producing cells in the local microvicinity.
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PMID:Early IL-4 production driving Th2 differentiation in a human in vivo allergic model is mast cell derived. 988 52

Renal interstitial fibrosis is the final common pathway leading to end-stage renal disease in various nephropathies including renal amyloidosis. However, the role of mast cells (MCs) in the fibrotic process of renal amyloidosis is not fully understood. We compared the distribution of MCs in renal biopsies from 30 patients with AA type renal amyloidosis and 20 control cases. Immunoreactivity of renal MCs to anti-tryptase and anti-chymase was studied. Interstitial myofibroblasts were stained with anti-alpha-smooth muscle actin (alpha-SMA) antibody, and inflammatory cells were identified by anti-CD45, -CD20, and -CD68 mAbs. Positively stained cells were counted, and the relative interstitial and fractional areas of anti-alpha-SMA stained cells were measured. Anti-CD29 mAb was used to detect beta1 integrin and anti-basic fibroblast growth factor (bFGF) mAb for the growth factor on MCs. MCs were rarely found in control samples. In contrast, samples showing amyloid deposition contained numerous tryptase-positive (MCT) (940.17 +/- 5.4 versus 6.74 +/- 1.1/mm2) but fewer chymase-positive (MCTC) cells (20.7 +/- 2.86 versus 1.7 +/- 0.76/mm2) in the renal interstitium. There was a significant relationship between interstitial MCT and creatinine clearance (r = -0.72), and between interstitial MCT and glomerular amyloid-index (GAI) (r = 0.723) and interstitial amyloid area (r = 0.824). Accumulation of MCs correlated significantly with the number of T lymphocytes (MCT: r = 0.694). There was also a significant relationship between mast cell (MC) number and the fractional area of alpha-SMA positive interstitium (r = 0.733) and interstitial fibrotic area (r = 0.6). Double immunostaining demonstrated intracytoplasmic presence of beta1 integrin on 87% of MCT and correlated significantly with the interstitial amyloid area (r = 0.818, P = .001) and T-cell number (r = 0.639, P = .002). bFGF was also detected on 85.5% of MCTC correlating well with the interstitial alpha-SMA-area (r = 0.789). Our results indicate that MCs constitute an integral part of the overall inflammatory process and play a crucial role in interstitial fibrosis in renal amyloidosis.
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PMID:Increased density of interstitial mast cells in amyloid A renal amyloidosis. 1100 43

Immunophenotyping has become an essential tool for diagnosis of hematological malignancies. By contrast, for diagnosis of Waldenstrom's macroglobulinemia (WM) immunophenotyping is used only occasionally. From 150 patients with a IgM monoclonal gammopathy we have selected 60 cases with (1) morphological lymphoplasmocytoid bone marrow (BM) infiltration (>20%); (2) IgM paraprotein (>10g/L); and (3) absence of features of other lymphoma types. Immunophenotypic analysis was based on the use of the triple or quadruple monoclonal antibody (MoAb) combinations. To increase the sensitivity of the analysis of antigen expression, selected CD19(+)CD20(+) B cells were targeted. We have also explored the antigenic characteristics of both the plasma cell (PC) and mast cell (MC) compartments present in the BM from 15 WM patients. Clonal WM lymphocytes were characterized by the constant expression of pan-B markers (CD19, CD20, CD22, CD24) together with sIg, predominantly kappa (5:1, kappa:lambda ratio). A high proportion of cases (75%) were positive for FMC7 and CD25, but in contrast to hairy cell leukemia (HCL), these lymphocytes were always negative for CD103 and CD11c. CD10 antigen was also absent in all WM patients and less than one fifth of patients were positive for CD5 and CD23, while CD27, CD45RA, and BCL-2 were present in most malignant cells. In two cases, the coexistence of two different clones of B lymphocytes was identified, and in eight additional cases, intraclonal phenotypic heterogeneity was observed. As far as PCs are concerned, in most patients (85%) the number of PCs was within the normal range (median, 0.36%). The antigenic profile of these PCs differed from that observed in normal and myelomatous PC (CD38(++)CD19(++/-)CD56(-)CD45(++)CD20(+)). In three cases, PCs showed aberrant expression for CD5, CD22, or FMC7. Finally, the number of mast cells was significantly higher (0.058 +/- 0.13) as compared to normal BM (0.019 +/- 0.02) (P <.01), although they were immunophenotypically normal (CD117(+)CD2(-)CD25(-)).
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PMID:Immunophenotypic analysis of Waldenstrom's macroglobulinemia. 1272 Jan 34

Atherosclerosis is considered a chronic inflammatory process, prompted by lipid accumulation and propagated by cell-mediated mechanisms. The present work was undertaken to clarify this process by characterizing cellular components of inflammatory infiltrate localized within atheroma. Cryostat sections of atherosclerotic lesions obtained from human carotid endarterectomy were analysed immunohistochemically by using monoclonal and polyclonal antibody directed against T cell subpopulations (CD3, CD4, CD8), B cells (CD20), plasma cells (CD138), macrophages (CD14), mast cells (anti-tryptase). Our results assess that T cells are the predominant cell type among plaque infiltrating inflammatory cells. B cells were detected near the lipid core of atheroma and clusters of plasma cells were observed within cellular infiltrates in most plaques. Numerous tryptase positive mast cells were noticed in many areas of complicated lesions. Our results indicate the presence of many inflammatory cells within type V and VI atherosclerotic plaques, suggesting the involvement of those cells in plaque progression. In fact it was previously shown that stability of atherosclerotic lesions is influenced by mast cell-released matrix metalloproteinases which induce plaque rupture and by cytokines and chemokines which increase local inflammatory response and are produced by lymphocytes and macrophages.
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PMID:Morphological analysis of cell subpopulations within carotid atherosclerotic plaques. 1610 Oct 28

Drug reactions can be considered as being either predictable or unpredictable. A predictable reaction would be the result of the pharmacologic action of the medication. An unpredictable reaction might be idiosyncratic, might be drug intolerance, or might have or imply an immunologic basis, such as being IgE mediated. Immediate reactions that are not IgE mediated can be considered as pseudoallergic (non-IgE-mediated mast cell activation). This review will discuss allergic and immunologic reactions to immunomodulators, penicillins and cephalosporins, sulfonamides, aspirin, and nonselective nonsteroidal anti-inflammatory drugs and consider the serious drug-related conditions of Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). The field of drug "allergy" has expanded to include adverse reactions associated with immunosuppressive medications, anticytokine therapies, and mAbs. The cytokine release reaction that occurs with anti-CD20 antibody infusions in patients with leukemia and white blood cell counts of greater than 50 x 10(9)/L is associated with high concentrations of TNF, IL-6, and IL-8. Because of the findings of fever, dyspnea, rigors, and hypotension, this reaction resembles the Jarisch-Herxheimer reaction that occurs 60 to 90 minutes after penicillin administration in patients with secondary syphilis. Furthermore, the care of the patient with penicillin allergy has been made more difficult in the absence of the major determinant, penicilloyl-polylysine, in that from 34% to 84% of patients who have positive skin test reactions to penicillin have exclusively positive reactions to the major determinant. SJS and TEN typically are caused by medications within 1 to 8 weeks of initiation of therapy. Evidence for death of the keratinocytes through (1) drug-specific cytotoxicity with the perforin-granzyme B-mediated killing and (2) activation of Fas on keratinocytes have provided explanations for the sloughing of skin. Unfortunately, intravenous immunoglobulin therapy for SJS and TEN has been disappointing.
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PMID:8. Drug allergy. 1645 48

Multiple myeloma oncogene 1/interferon regulatory factor 4 (MUM1/IRF4) is involved in lymphoid cell differentiation, particularly in the production of plasma cells. We examined the immunoreactivity of mouse monoclonal antibody Mum-1p to MUM1/IRF4 and compared it with expression of CD79a and CD20 in 109 plasmacytomas in 107 dogs. Tissues had been fixed in formalin and embedded in paraffin. One hundred one of 109 (93.5%) tumors were positive for MUM1/IRF4. The staining was nuclear with weak cytoplasmic reaction. Fifty-nine of 105 (56.2%) plasmacytomas were positive for CD79a; only 21 of 108 (19.4%) cases were positive for CD20. MUM1/IRF4 staining was performed on 139 other tumors including B- and T-cell lymphomas, histiocytic proliferations, mast cell tumors, and melanocytic tumors. The only MUM1/IRF4-positive nonplasmacytic tumors were 10 B-cell lymphomas and 1 anaplastic lymphoma. We conclude the following: 1) Antibody Mum-1p is very specific for canine plasmacytomas, 2) antibody Mum-1p is superior in sensitivity and specificity to CD79a and CD20 for the identification of canine plasmacytomas in formalin-fixed, paraffin-embedded tissues, 3) canine lymphomas that express MUM1/IRF4 are few and usually of B-cell origin, 4) other canine leukocytic and melanocytic tumors do not express MUM1/IRF4, and 5) prospective studies are needed to determine whether the expression of MUM1/IRF4, particularly in lymphomas, has prognostic significance.
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PMID:Immunohistochemical detection of multiple myeloma 1/interferon regulatory factor 4 (MUM1/IRF-4) in canine plasmacytoma: comparison with CD79a and CD20. 1803

Patients with systemic mastocytosis (SM) may acquire an associated hematologic non-mast cell (MC)-lineage disease (AHNMD). In most cases, a myeloid neoplasm is diagnosed, whereas the occurrence of a lymphoproliferative disease is an extremely rare event. We report on a patient with indolent SM associated with small lymphocytic lymphoma (SLL). The patient presented with lymphadenopathy, maculopapular exanthema, and elevated serum tryptase. The bone marrow biopsy showed focal MC aggregates together with SLL. As assessed by immunostaining, neoplastic MC were found to exhibit CD117 and CD25 but did not display CD5 or CD20, whereas SLL cells were found to coexpress CD5 and CD20 but did not express MC antigens. The KIT mutation D816V was detected in sorted CD34(+) cells and unfractionated marrow cells but not in CD5(+) SLL cells, confirming the coexistence of 2 distinct neoplasms.
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PMID:Indolent systemic mastocytosis associated with atypical small lymphocytic lymphoma: a rare form of concomitant lymphoproliferative disease. 1844 46

We aimed to investigate the profile of the inflammatory infiltrate in lesional and nonlesional tissue in alopecia areata (AA) and look for possible associations between inflammatory mechanisms, neuropeptide expressions, and various clinical features. Twenty-four patch-type AA patients were included. Forty-eight lesional and nonlesional skin samples were stained immunohistochemically with antibodies for CD1a, CD3, CD4, CD8, CD20, CD57 (for natural killer cells), mast cell tryptase, nerve growth factor receptor (NGFR), and substance P (SP). Various clinical findings were recorded. Psychological distress levels and stress-related hormones were measured. Lesional skin showed statistically more CD3(+), CD8(+), and CD57(+) lymphocytes, mast cells, Langerhans cells, and more prominent immunoreactivities of NGFR and SP (P < 0.003). Most nonlesional skin showed CD3(+) and CD57(+) cells, mast cells, and NGFR(+) nerve fibers. NGFR and SP, and SP and perivascular mast cell infiltrates were correlated, whereas peribulbar mast cells and anagen follicle counts were inversely correlated in nonlesional skin (P < 0.05). Near half of the patients' distress levels were high. No relationship among biochemical, psychological, and clinical parameters could be shown. AA may involve the entire skin in which lesions occur as a result of local T cell-mediated cytotoxic inflammatory response initiated by Langerhans cells and mast cells activated via neuropeptides.
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PMID:Investigation of the inflammatory mechanisms in alopecia areata. 1915 26


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