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Titlebook: Current Topics in Complement II; John D. Lambris Book 2008 The Editor(s) (if applicable) and The Author(s), under exclusive license to Spr

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發(fā)表于 2025-3-21 17:33:19 | 只看該作者 |倒序?yàn)g覽 |閱讀模式
書(shū)目名稱Current Topics in Complement II
編輯John D. Lambris
視頻videohttp://file.papertrans.cn/242/241349/241349.mp4
概述Proceedings from the Fourth Aegean Conferences Workshop on Complement Associated Diseases, Animal Models, and Therapeutics (June 10-15, 2007)
叢書(shū)名稱Advances in Experimental Medicine and Biology
圖書(shū)封面Titlebook: Current Topics in Complement II;  John D. Lambris Book 2008 The Editor(s) (if applicable) and The Author(s), under exclusive license to Spr
描述.Complement has long been regarded as a pivotal effector arm of the innate immune response, eliciting important immunoregulatory functions in the context of inflammation and also serving as a vital link between the innate and adaptive immune response. In the post-genomic era, our knowledge of the innate immune system is enriched by findings that point to novel functions that do not strictly correlate with immunological defense and surveillance, immune modulation or Inflammation. Several studies indicate that complement proteins exert functions that are either more complex than previously thought, or go well beyond the innate immune character of the system. The advent of high-throughput platforms for genome and proteome-wide profiling, together with the enormous amount of raw genetic information that has accumulated in the databases, have stirred new expectations in biomedical research. They have led complementologists to revisit established biological systems, such as the complement system, from a global and integrative perspective. Complement research is now faced with the challenge of trying to integrate isolated biochemical pathways into complex gene and protein regulatory circu
出版日期Book 2008
關(guān)鍵詞autoimmune disease; bacteria; physiology; protein; virus; infectious diseases
版次1
doihttps://doi.org/10.1007/978-0-387-78952-1
isbn_softcover978-1-4419-2706-4
isbn_ebook978-0-387-78952-1Series ISSN 0065-2598 Series E-ISSN 2214-8019
issn_series 0065-2598
copyrightThe Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Science+Busines
The information of publication is updating

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978-1-4419-2706-4The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Science+Busines
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John D. LambrisProceedings from the Fourth Aegean Conferences Workshop on Complement Associated Diseases, Animal Models, and Therapeutics (June 10-15, 2007)
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Advances in Experimental Medicine and Biologyhttp://image.papertrans.cn/d/image/241349.jpg
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The Minerals, Metals & Materials Seriese response. C3a, C5a and their receptors have been revealed to be present in the central nervous system (CNS) as well as the peripheral immune system. We found that centrally administered C3a suppresses food intake, while C5a stimulates food intake, and their food intake regulation may be associated
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Bug Reports Evolution in Open Source Systemsse. Complement activation mediated by anti-tumor mAbs can result in direct tumor lysis or enhancement of antibody-dependent cellular cytotoxicy. Chemotaxis of phagocytic cells by complement activation products C5a is also required for certain cancer immunotherapy such as combined β -glucan with anti
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https://doi.org/10.1007/978-3-319-78753-4ng disease. Here we review subversive interactions of Porphyromonas gingivalis, a major periodontal pathogen, with the complement receptor-3 (CR3; CD11b/CD18) in monocytes/macrophages. Through its cell surface fimbriae, P. gingivalis stimulates Toll-like receptor-2 (TLR2) inside-out signaling which
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