-
-
[1]Joplin RE, Neuberger JM.Immunopathology of primary biliary cir-rhosis[J].Gastroenterol Hepatol, 1999, 11 (6) ∶587-593. [2]Jiang XH, Zhong RQ, Fang XY.Establishment of a mouse model ofprimary biliary cirrhosis by AMAM2 autoantigen injection[J].Zhon-ghua Gan Zang Bing Za Zhi, 2006, 14 (3) ∶202-204. [3]Mackay IR.Hepatoimmunology:a perspective[J].Immunol Cell Bi-ol, 2002, 80 (1) ∶36-44. [4]Ballot E, Bandin O, Chazouilleres O, et al.Immune response to li-popolysaccharide in primary biliary cirrhosis and autoimmune disea-ses[J].J Autoimmun, 2004, 22 (2) ∶153-158. [5]Selmi C, Invernizzi P, Keeffe EB, et al.Epidemiology and patho-genesis of primary biliary cirrhosis[J].J Clin Gastroenterol, 2004, 38 (3) ∶264-271. [6]Abdulkarim AS, Petrovic LM, Kim WR, et al.Primary biliary cir-rhosis:an infectious disease caused by Chlamydia pneumoniae[J]?J Hepatol, 2004, 40 (3) ∶380-384. [7]Nishio A, Keeffe EB, Gershwin ME.Immunopathogenesis of primarybiliary cirrhosis[J].Semin Liver Dis, 2002, 22 (3) ∶291-302. [8]Wang AP, Migita K, Masahiro I, et al.Hepatic expression of toll-like receptor 4 in primary biliary cirrhosis[J].J Autoimmun, 2005, 25∶85-91. [9]Harada K, Ohira S, Isse K, et al.Lipopolysaccharide activates nu-clear factor-kappaB through toll-like receptors and related mole-cules in cultured biliary epithelial cells[J].Lab Invest, 2003, 83∶1657-1667. [10]Kikuchi K, Lian ZX, Kimura Y, et al.Genetic polymorphisms oftoll-like receptor 9 influencethe immune response to CpG and con-tribute to hyper-IgMin primary biliary cirrhosis[J].J Autoimmun, 2005, 24 (4) ∶347-352. [11]HarutaⅠ, Hashimoto E, Kato Y, et al.Lipoteichoic acid may af-fect the pathogenesis of bile duct damage in primary biliarycirrhosis[J].Autoimmunity, 2006, 39 (2) ∶129-135. [12]Kaplan MM.Novosphingobium aromaticivorans:a potential initiatorof primary biliary cirrhosis[J].Am J Gastroenterol, 2004, 99 (11) ∶2147-2149. [13]Kita H, Matsumura S, He XS, et al.Quantitation and functional a-nalysis of PDC-E2 specific autoreactive cytotoxic T lymphocytes inprimary biliary cirrhosis[J].J Clin Invest, 2002, 109 (9) ∶1231-1240. [14]Kita H, Lian ZX, Vande WJ, et al.Identification of HLA-A2 re-stricted CD8+cytotoxic T cell responses in primary billary cirrho-sus:Tcell activation is augmented by immune complex cross-pres-ented by dendritic cells[J].J Exp Med, 2002, 195∶113-123. [15]Isse K, Harada K, Sato Y, et al.Characterization of biliary intra-epithelial lymphocytes at different anatomical levels of intrahepaticbile ducts under normal and pathological conditions:numbers of CD4+CD28-intra-epithelial lymphocytes are increased in primarybiliary cirrhosis[J].Pathol Int, 2006, 56 (1) ∶17-24. [16]Stone J, Wade JA, Cauch DK, et al.Human leukocyte antigenclassⅡassociation in serumantimitochomdrial antibodies (AMA) -positive and AMA-negative primary biliary cirrhosis[J].J Hepa-tolgy, 2002, 36∶8-13. [17]姜小华, 仲人前, 方晓云, 等.原发性胆汁性肝硬化与HLA-DRB1、DQB1等位基因的相关性研究[J].中华肝脏病杂志, 2004, 12∶436. [18]Matsushita M, Tanaka A, Kikuchi K, et al.Association of singlenucleotide polymorphisms of the interleukin-10 promoter gene andsusceptibility to primary biliary cirrhosis:immunogenetic differencesin Italian and Japanese patients[J].Autoimmunity, 2002, 35∶531-536.
本文二维码
计量
- 文章访问数: 3328
- HTML全文浏览量: 1
- PDF下载量: 1001
- 被引次数: 0