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病毒性肝炎的发病机理较为复杂,一般认为肝炎病毒本身引起细胞病变的能力较小,而机体免疫反应对肝炎的发病有重要作用。早在1969年 Almeida 首先提出免疫复合物损伤在肝炎发病机制中起重要作用。近年来有关病毒性肝炎中免疫复合物的形成机理、检测方法及其与临床的关系国内外已有不少报道。兹将有关的研究资料概述如下。病理性免疫复合物的形成机理当抗原与抗体相互作用时产生了免疫复合物。病理性的免疫复合物为19S 中等大小的分子颗粒,抗原抗体比例为3∶2。不仅可以激活补体系统,产生一系列介质,并可激活凝血、纤溶和缓激肽等系统。这些系统相互激活、相互抑制而参与炎症反应,其产物还可作
The pathogenesis of viral hepatitis is more complicated, it is generally believed that the hepatitis C virus itself has a lesser ability to cause cytopathic effects, and the immune response to the body plays an important role in the pathogenesis of hepatitis. As early as 1969, Almeida first proposed that immune complex damage plays an important role in the pathogenesis of hepatitis. In recent years, the formation mechanism of immune complexes in viral hepatitis, detection methods and clinical and its relationship with many reports at home and abroad. The relevant research materials are summarized below. Pathogenesis of immunocomplex formation mechanism When the antigen and antibody interact to produce immune complexes. Pathological immune complexes are 19S medium sized molecular particles, antigen-antibody ratio of 3: 2. It not only activates the complement system, producing a range of media, but also activates systems such as coagulation, fibrinolysis, and bradykinin. These systems activate each other, inhibit each other and participate in the inflammatory response, the product can be made