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Titlebook: Mechanisms of B Cell Neoplasia 1998; Proceedings of the W Fritz Melchers,Michael Potter Conference proceedings 1999 The Editor(s) (if appli

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书目名称Mechanisms of B Cell Neoplasia 1998
副标题Proceedings of the W
编辑Fritz Melchers,Michael Potter
视频video
概述Includes supplementary material:
丛书名称Current Topics in Microbiology and Immunology
图书封面Titlebook: Mechanisms of B Cell Neoplasia 1998; Proceedings of the W Fritz Melchers,Michael Potter Conference proceedings 1999 The Editor(s) (if appli
描述Workshops on the mechanisms of B cell neoplasia have been organized alternatively in Bethesda and Basel since 1983. Prog­ ress in our understanding of the development and responses of B lymphocytes is presented and discussed with the aim and hope to understand what might go wrong when B lymphocytes are transformed into malignant cells. Such knowledge might lead to better diagnosis, prevention and even cure of these terri­ ble diseases. The presentations at the Bethesda workshops are published as papers in volumes of Current Topics in Microbiol­ ogy and Immunology, while the presentations and discussions in Basel were transcribed and published in Editions Roche. For the first time, a Basel workshop (held 4th-6th October 1998) that has been recorded and, in part, transcribed is being published as papers and discussions within Current Topics. This volume is the latest of a long series which documents the excitements of ground-breaking discoveries as well as the frustrations of our inability to fully understand the mechanisms leading to B cell neoplasia. The papers at the workshop are presented when possible in the sequence in which they were given. However, to facilitate the organizat
出版日期Conference proceedings 1999
关键词AIDS; Chemokine; DNA; apoptosis; autoimmunity; bacteria; cell; immunity; leukemia; lymphocytes; lymphoma; mutag
版次1
doihttps://doi.org/10.1007/978-3-642-60162-0
isbn_softcover978-3-642-64283-8
isbn_ebook978-3-642-60162-0Series ISSN 0070-217X Series E-ISSN 2196-9965
issn_series 0070-217X
copyrightThe Editor(s) (if applicable) and The Author(s), under exclusive license to Springer-Verlag GmbH, DE
The information of publication is updating

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Negative Selection of Self-reactive B Lymphocytes Involves Complement For example, mice bearing targeted disruption of molecules involved in regulation of BCR signaling such as CD22, SHP-1 (Cyster et al. 1995), CD45 (Cyster et al. 1996) or Lyn (Cornall et al. 1998) have altered negative selection of self-reactive B cells in the sHEL/HEL-Ig double tg model. Alternativ
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Cross-talk Between CD44 and c-Met in B cellseceptor ligation. Stimulation of c-Met with HGF/SF, which is produced at high levels by tonsillar stromal cells and FDC, leads to enhanced integrin-mediated adhesion of B cells to fibronectin and VCAM-1 [22].
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Role of Complement Receptors CD21/CD35 in B Lymphocyte Activation and Survivalplement and is particularly important in recognition of protein antigens in addition to carbohydrate. For the purposes of this review, the enhancing effect of complement is most probably mediated by natural IgM, as deficiency in secretory IgM results in an impaired B cell response to suboptimal dose
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Chemokines and B-cell Homing to Folliclesin humans (Birkenbach et al. 1993; Dobner et al. 1992). To track expression of the mouse receptors, the amino-terminal ectodomains were expressed as GST fusion proteins and used to immunize rabbits. An antiserum against BLR1 was isolated and affinity purified using the same BLR1 fragment expressed a
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R. A. Manz,G. Cassese,A. Thiel,A. Radbruch hopes that the young scientists of the next generation will be enthusiastically inspired by this book and will develop the field of organic semiconductors even further..978-981-99-1239-1978-981-99-1237-7Series ISSN 1386-3290
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C. Schaniel,F. Sallusto,P. Sideras,F. Melchers,A. G. Rolinkoducts and systems. The chapters in this book may further give impetus to explore new avenues leading towards multidisciplinary research discussions associatedwith the resilience and sustainability of the existing systems..978-981-99-1523-1978-981-99-1521-7Series ISSN 2731-4049 Series E-ISSN 2731-4057
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