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Titlebook: Immunological Aspects of Liver Disease; Howard C. Thomas,Peter A. Miescher,Hans J. Mueller Book 1982 Springer-Verlag Berlin Heidelberg 198

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發(fā)表于 2025-3-21 17:49:25 | 只看該作者 |倒序瀏覽 |閱讀模式
書目名稱Immunological Aspects of Liver Disease
編輯Howard C. Thomas,Peter A. Miescher,Hans J. Mueller
視頻videohttp://file.papertrans.cn/463/462179/462179.mp4
圖書封面Titlebook: Immunological Aspects of Liver Disease;  Howard C. Thomas,Peter A. Miescher,Hans J. Mueller Book 1982 Springer-Verlag Berlin Heidelberg 198
描述Howard C. Thomas In normal subjects the regulatory apparatus of the immune system permits responses to foreign antigens but suppresses those directed to "self‘ components. Autoimmune disease occurs as a failure ofthis system either as a result of a primary defect in the regulatory apparatus (primary autoimmunization) or because of a change in the antigenicity of the tissues (secondary autoimmunization). Autoaggressive reactions are characterised by the presence of autoantibodies. When these are directed to membrane displayed antigens (Fig. 1) they are probably of importance in the lysis of hepatocytes. Those directed to cytoplasmic antigens may be useful diagnostically but are of unknown pathogenic significance. When no extrinsic aetiological factor can be identified, the process is assumed to be the result of a failure ofthe regulatory system, allowing the spontaneous expansion of a clone of autoreactive lymphocytes. The defect may be generalised or specific to certain groups of self-antigens and thus the autoimmune disease may be either multi- or unisystemic. The recent development of techniques to enumerate and measure the functional activity of the suppressor lymphocytes which
出版日期Book 1982
關鍵詞Antigen; autoimmune disease; cancer; diseases; hepatitis; hepatitis B; immunology; infection; liver; liver di
版次1
doihttps://doi.org/10.1007/978-3-642-68446-3
isbn_softcover978-3-540-11310-2
isbn_ebook978-3-642-68446-3
copyrightSpringer-Verlag Berlin Heidelberg 1982
The information of publication is updating

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發(fā)表于 2025-3-21 21:09:59 | 只看該作者
Book 1982to "self‘ components. Autoimmune disease occurs as a failure ofthis system either as a result of a primary defect in the regulatory apparatus (primary autoimmunization) or because of a change in the antigenicity of the tissues (secondary autoimmunization). Autoaggressive reactions are characterised
板凳
發(fā)表于 2025-3-22 04:18:06 | 只看該作者
Drug-Induced Chronic Hepatitis,. All individuals are susceptible, the lesion is reproducible in animals and there is a direct dose relationship. Even after severe hepatic necrosis, should the patient survive, agents producing a direct hepatotoxic reaction seldom lead to a chronic lesion.
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Genetic Determinants of Autoimmune Chronic Active Hepatitis,lity antigens, of relevance to tissue transplantation, and associations between certain immunopathic diseases and HLA specificities [26, 31]. However, despite much experimental work and theoretical speculation, no unifying concept relating MHC-linked Ir genes effects and MHC- linked disease susceptibility has yet emerged.
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Immunopathogenesis of the Extrahepatic Manifestations of Hepatitis B Virus Infection,ese syndromes and their comparison with animal models of immune complex injury, we have made progress in understanding the pathogenesis of these extrahepatic features; however, many important questions about the association among HBV, immune complexes, and extrahepatic tissue injury remain unanswered.
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Pathogenic Mechanisms in Primary Biliary Cirrhosis,moral immunity. Patients exhibit a generalised state of immune hyporesponsiveness being anergic to DNCB [15] and producing a diminished antibody response to parenteral antigenic challenge [16, 57]. They also exhibit failure of the immune response to convert from IgM to IgG antibody synthesis [57].
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