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  • 1
    Online Resource
    Online Resource
    S. Karger AG ; 2002
    In:  International Archives of Allergy and Immunology Vol. 127, No. 2 ( 2002), p. 140-142
    In: International Archives of Allergy and Immunology, S. Karger AG, Vol. 127, No. 2 ( 2002), p. 140-142
    Abstract: Systemic mastocytosis (SM) is a myeloproliferative disease affecting multipotent and/or mast cell-committed hematopoietic progenitor cells. In a significant subgroup of patients (10–35%), an associated clonal hematologic non-mast cell lineage disorder (AHNMD) occurs. These AHNMDs can be classified according to recently established WHO criteria. Most AHNMDs resemble myeloid malignancies such as acute myeloid leukemia, myeloproliferative disorders or myelodysplastic syndromes. In only a few cases, lymphoproliferative disorders are diagnosed. Patients with SM-AHNMD have a less favorable prognosis concerning survival when compared to indolent SM. No general guidelines for the treatment of patients with SM-AHNMD have been established so far. A reasonable straightforward approach may be to treat the AHNMD in those patients in the same way as if no coexisting SM exists.
    Type of Medium: Online Resource
    ISSN: 1018-2438 , 1423-0097
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2002
    detail.hit.zdb_id: 1482722-0
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  • 2
    In: International Archives of Allergy and Immunology, S. Karger AG, Vol. 120, No. 2 ( 1999), p. 108-116
    Abstract: We have previously reported that patients suffering from atopic dermatitis (AD) frequently display IgE autoantibody reactivity to human proteins expressed in cell lines of different histogenetic origins. Molecular cloning and in situ staining experiments revealed that certain IgE–reactive autoantigens were expressed preferentially in target organs of atopy while others could be detected in various tissues and cell types. Here we use serum IgE from AD patients to investigate the distribution of autoantigens in subcellular fractions of the human epithelial cell line A431 and in human tissue specimens. Results obtained showed that IgE–reactive autoantigens can be detected in the nuclear 〉 microsomal 〉 mitochondrial 〉 cytoplasmic fraction of A431 cells as well as in a variety of human tissue specimens (brain, bone, intestine, liver, lung, muscle, skin, uterus) and effector cells of atopy (basophils, mast cells, T cells). If IgE autoreactivity plays a pathogenetic role in severe forms of atopy, organ–specific manifestations (e.g. AD) may result from the transport to and deposition of IgE–reactive autoantigens in certain target organs (skin) rather than from a preferential expression of the autoantigens in the affected tissues.
    Type of Medium: Online Resource
    ISSN: 1018-2438 , 1423-0097
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 1999
    detail.hit.zdb_id: 1482722-0
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  • 3
    Online Resource
    Online Resource
    S. Karger AG ; 1999
    In:  International Archives of Allergy and Immunology Vol. 120, No. 1 ( 1999), p. 1-7
    In: International Archives of Allergy and Immunology, S. Karger AG, Vol. 120, No. 1 ( 1999), p. 1-7
    Abstract: The term mastocytosis denotes a heterogenous group of disorders characterized by abnormal growth and accumulation of mast cells in one or more organs. Cutaneous and systemic variants of the disease have been described. Mast cell disorders have also been categorized according to other aspects, such as family history, age, course of disease, or presence of a concomitant myeloid neoplasm. However, so far, generally accepted disease criteria are missing. Recently, a number of diagnostic (disease–related) markers have been identified in mastocytosis research. These include the mast cell enzyme tryptase, CD2, and mast cell growth factor receptor c–kit (CD117). Several gain–of–function–mutations in the kinase domain of c–kit appear to occur in mastocytosis supporting the clonal (neoplastic) nature of the disease. Also, certain point mutations appear to be associated with distinct variants of mastocytosis, i.e. Asp–816→Val with a subset of sporadic persistent (systemic) mastocytosis (mostly adults), and Gly–839→Lys with (a subset of) typical pediatric (mostly cutaneous) mastocytosis. Another potential indicator of mast cell neoplasm is the T–/NK–cell–associated marker CD2. This antigen (LFA–2) is abnormally expressed on neoplastic mast cells in cases of systemic mastocytosis or mast cell leukemia, but not found on normal mast cells. The mast cell enzyme tryptase is increasingly used as a serum– and immunohistochemical marker to estimate the actual spread of disease (burden of neoplastic mast cells). The clinical significance of novel mastocytosis markers is currently under investigation. First results indicate that they may be useful to define reliable criteria for the delineation of the disease.
    Type of Medium: Online Resource
    ISSN: 1018-2438 , 1423-0097
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 1999
    detail.hit.zdb_id: 1482722-0
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  • 4
    Online Resource
    Online Resource
    S. Karger AG ; 2002
    In:  International Archives of Allergy and Immunology Vol. 127, No. 2 ( 2002), p. 137-139
    In: International Archives of Allergy and Immunology, S. Karger AG, Vol. 127, No. 2 ( 2002), p. 137-139
    Abstract: Systemic mastocytosis (SM) is a clonal disease that shows an either indolent or an aggressive clinical course. Utilizing established criteria, indolent SM can readily be discriminated from the rare aggressive subvariants of SM in most cases. In a small group of patients, however, clinical and laboratory parameters are indicative of slow progression without signs of aggressive disease or an associated hemopoietic neoplasm. These SM patients exhibit a high burden of mast cells, hypercellular marrow and organomegaly. Because of the ‘intermediate’ course and uncertain prognosis, these cases have been referred to as smouldering SM. In the present article, we discuss clinical and laboratory findings in smouldering SM and review the current literature. In addition, the pathophysiology of this novel subtype of SM is discussed.
    Type of Medium: Online Resource
    ISSN: 1018-2438 , 1423-0097
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2002
    detail.hit.zdb_id: 1482722-0
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  • 5
    Online Resource
    Online Resource
    S. Karger AG ; 1990
    In:  International Archives of Allergy and Immunology Vol. 91, No. 2 ( 1990), p. 198-203
    In: International Archives of Allergy and Immunology, S. Karger AG, Vol. 91, No. 2 ( 1990), p. 198-203
    Abstract: Recently, we were able to establish the immunologic surface marker profile of human basophils and mast cells. In the present study, the characterization of these cell types was extended by the use of monoclonal antibodies (mAbs) to hemopoietic differentiation antigens. Basophils and mast cells were enriched by mAbs and complement from chronic myeloid leukemia blood (n = 5) and dispersed lung tissue (n = 4), respectively. A panel of 80 mAbs was tested for being reactive with purified cell populations using flow cytometry and/or a combined toluidine blue-immunofluorescence staining procedure. In addition to previous findings, basophils were found to react with mAbs directed against the 126-kilodalton dipeptidylpeptidase IV (CD26), platelet glycoprotein IIa (CD31), CD40 antigen known to share sequence homology with nerve growth factor receptor, leukosialin (CD43), CD44 antigen, the ICAM-1 antigen (CD54) and VIM2-reactive gangliosides involving the sialofucooligosaccharide sequence (CDw65L). Bsp-1 was found to be a specific marker for human basophils, whereas mast cells were not stained by this reagent. Basophils apparently lack CD22 antigen, gangliosides detected by CDw65 mAbs (except CDw65L) and CD71 antigen (transferrin receptor). Mast cells were found to express CD43 and CD44 antigen. In contrast, mast cells lack CD22, CD26, CD31, CD40 and CDw65 antigen. These results provide further evidence that both blood basophils and mast cells express a unique immunologic surface marker profile including binding sites for a variety of immunomodulating ligands and adhesion molecules.
    Type of Medium: Online Resource
    ISSN: 1018-2438 , 1423-0097
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 1990
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  • 6
    In: International Archives of Allergy and Immunology, S. Karger AG, Vol. 157, No. 3 ( 2012), p. 215-225
    Abstract: Activation of tissue mast cells (MCs) and their abnormal growth and accumulation in various organs are typically found in primary MC disorders also referred to as mastocytosis. However, increasing numbers of patients are now being informed that their clinical findings are due to MC activation (MCA) that is neither associated with mastocytosis nor with a defined allergic or inflammatory reaction. In other patients with MCA, MCs appear to be clonal cells, but criteria for diagnosing mastocytosis are not met. A working conference was organized in 2010 with the aim to define criteria for diagnosing MCA and related disorders, and to propose a global unifying classification of all MC disorders and pathologic MC reactions. This classification includes three types of ‘MCA syndromes’ (MCASs), namely primary MCAS, secondary MCAS and idiopathic MCAS. MCA is now defined by robust and generally applicable criteria, including (1) typical clinical symptoms, (2) a substantial transient increase in serum total tryptase level or an increase in other MC-derived mediators, such as histamine or prostaglandin D 〈 sub 〉 2 〈 /sub 〉 , or their urinary metabolites, and (3) a response of clinical symptoms to agents that attenuate the production or activities of MC mediators. These criteria should assist in the identification and diagnosis of patients with MCAS, and in avoiding misdiagnoses or overinterpretation of clinical symptoms in daily practice. Moreover, the MCAS concept should stimulate research in order to identify and exploit new molecular mechanisms and therapeutic targets.
    Type of Medium: Online Resource
    ISSN: 1018-2438 , 1423-0097
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2012
    detail.hit.zdb_id: 1482722-0
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  • 7
    Online Resource
    Online Resource
    S. Karger AG ; 2002
    In:  International Archives of Allergy and Immunology Vol. 127, No. 2 ( 2002), p. 115-117
    In: International Archives of Allergy and Immunology, S. Karger AG, Vol. 127, No. 2 ( 2002), p. 115-117
    Abstract: The diagnosis of mastocytosis is based on histological evidence of a focal increase in tissue mast cells. Immunohistochemical staining with antitryptase antibodies is strongly recommended in all cases of suspected mastocytosis because mast cell infiltrates may be small and scanty. Mastocytosis may be difficult to distinguish from other hematological malignancies, in which an increase in mast cells is frequently seen. The expression of the T cell-associated antigen CD2 has been shown to be exclusively found on neoplastic mast cells in mastocytosis. The demonstration of expression of vascular endothelial growth factor by mast cells is consistent with the finding of angiogenesis which is commonly seen in tissue infiltrates of mastocytosis.
    Type of Medium: Online Resource
    ISSN: 1018-2438 , 1423-0097
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2002
    detail.hit.zdb_id: 1482722-0
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  • 8
    In: International Archives of Allergy and Immunology, S. Karger AG, Vol. 116, No. 3 ( 1998), p. 167-176
    Abstract: The interaction of immunoglobulin E and otherwise harmless antigens (allergens) leadsin sensitized individuals through effector cell activation to the immediate induction of acascade of inflammatory reactions, the hallmark of type I allergy. Recently, the molecularand structural characterization of allergens, specific IgE antibodies and their epitopes hasmade rapid progress. Here we discuss active and passive strategies for therapy of type Iallergy, which are based on interfering with the IgE–allergen interaction.
    Type of Medium: Online Resource
    ISSN: 1018-2438 , 1423-0097
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 1998
    detail.hit.zdb_id: 1482722-0
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  • 9
    Online Resource
    Online Resource
    S. Karger AG ; 1996
    In:  International Archives of Allergy and Immunology Vol. 110, No. 3 ( 1996), p. 252-260
    In: International Archives of Allergy and Immunology, S. Karger AG, Vol. 110, No. 3 ( 1996), p. 252-260
    Type of Medium: Online Resource
    ISSN: 1018-2438 , 1423-0097
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 1996
    detail.hit.zdb_id: 1482722-0
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  • 10
    Online Resource
    Online Resource
    S. Karger AG ; 2011
    In:  International Archives of Allergy and Immunology Vol. 155, No. 3 ( 2011), p. 306-308
    In: International Archives of Allergy and Immunology, S. Karger AG, Vol. 155, No. 3 ( 2011), p. 306-308
    Type of Medium: Online Resource
    ISSN: 1423-0097 , 1018-2438
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2011
    detail.hit.zdb_id: 1482722-0
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