Recent advances in the concept and pathogenesis of IgG4-related disease in the hepato-bilio-pancreatic system.
Recent advances in the concept and pathogenesis of IgG4-related disease in the hepato-bilio-pancreatic system.
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DOI：
10.5009/gnl14107
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发表时间：
2014-09
期刊：
影响因子：
3.4
通讯作者：
Uchida K
中科院分区：
文献类型：
--
作者：
Okazaki K;Yanagawa M;Mitsuyama T;Uchida K
最近的研究提出将1型自身免疫性胰腺炎（AIP） （igg4相关胰腺炎）、igg4相关硬化性胆管炎（IgG4-SC）、igg4相关胆囊炎和igg4相关肝病命名为肝胆胰系统中的igg4相关疾病（IgG4-RD）。在igg4相关肝病中，提出了与AIH具有相同组织病理学特征的igg4相关自身免疫性肝炎（AIH）的新概念。在IgG4-RD涉及的器官中，最常观察到与胰腺和胆道病变相关的器官，这支持了“胆道疾病伴胰腺病变”的新概念。1型AIP和IgG4-SC的靶点可能是胆汁和胰管周围的管周腺。基于遗传背景，先天免疫和获得性免疫、th2显性免疫状态、调节性T （Treg）或B细胞以及补体激活等经典途径可能参与IgG4-RD的发展。尽管IgG4在IgG4- rd中的作用尚不清楚，但来自Treg细胞的白介素10和来自单核细胞/嗜碱性粒细胞的B细胞活化因子通过toll样受体/核苷酸结合寡聚结构域样受体的刺激，上调了IgG4的产生。基于这些发现，我们提出了IgG4-RD在肝胆胰系统中发展的假设。IgG4-RD的致病机制有待进一步研究。
Recent studies have proposed nomenclatures of type 1 autoimmune pancreatitis (AIP) (IgG4-related pancreatitis), IgG4-related sclerosing cholangitis (IgG4-SC), IgG4-related cholecystitis, and IgG4-related hepatopathy as IgG4-related disease (IgG4-RD) in the hepato-bilio-pancreatic system. In IgG4-related hepatopathy, a novel concept of IgG4-related autoimmune hepatitis (AIH) with the same histopathological features as AIH has been proposed. Among organs involved in IgG4-RD, associations with pancreatic and biliary lesions are most frequently observed, supporting the novel concept of “biliary diseases with pancreatic counterparts.” Targets of type 1 AIP and IgG4-SC may be periductal glands around the bile and pancreatic ducts. Based on genetic backgrounds, innate and acquired immunity, Th2-dominant immune status, regulatory T (Treg) or B cells, and complement activation via a classical pathway may be involved in the development of IgG4-RD. Although the role of IgG4 remains unclear in IgG4-RD, IgG4-production is upregulated by interleukin 10 from Treg cells and by B cell activating factor from monocytes/basophils with stimulation of toll-like receptors/nucleotide-binding oligomerization domain-like receptors. Based on these findings, we have proposed a hypothesis for the development of IgG4-RD in the hepato-bilio-pancreatic system. Further studies are necessary to clarify the pathogenic mechanism of IgG4-RD.
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