[1] Tanaka A, Takikawa H, Miwa H, et al. Changing nomenclature for PBC from "primary biliary cirrhosis" to "primary biliary cholangitis". Hepatol Res, 2016,46: 725-726. [2] Wang L, Gershwin M E, Wang F. Primary biliary cholangitis in China. Curr Opin Gastroenterol, 2016, 32:195-203 [3] Liu H, Liu Y, Wang L, et al. Prevalence of primary biliary cirrhosis in adults referring hospital for annual health check-up in Southern China. BMC Gastroenterol, 2010,10: 100. [4] Lindor KD, Bowlus CL, Boyer J, et al. Primary Biliary Cholangitis: 2018 Practice Guidance from the American Association for the Study of Liver Diseases. Hepatology, 2018, 69:1-51. [5] Yang CY, Ma X, Tsuneyama K, et al. IL-12/Th1 and IL-23/Th17 biliary microenvironment in primary biliary cirrhosis: implications for therapy. Hepatology, 2014,59: 1944-1953. [6] Lan RY, Salunga TL, Tsuneyama K, et al. Hepatic IL-17 responses in human and murine primary biliary cirrhosis. J Autoimmun, 2009,32: 43-51. [7] Nakagawa R, Muroyama R, Saeki C, et al. CD4(+) T cells from patients with primary biliary cholangitis show T cell activation and differentially expressed T-cell receptor repertoires. Hepatol Res, 2019,49: 653-662. [8] Watanabe S, Yamada Y, Murakami H. Expression of Th1/Th2 cell-related chemokine receptors on CD4(+) lymphocytes under physiological conditions. Int J Lab Hematol, 2020,42: 68-76. [9] Guggino G, Giardina AR, Raimondo S, et al. Targeting IL-6 signalling in early rheumatoid arthritis is followed by Th1 and Th17 suppression and Th2 expansion. Clin Exp Rheumatol, 2014,32: 77-81. [10] Raveney BJ, Oki S, Yamamura T. Nuclear receptor NR4A2 orchestrates Th17 cell-mediated autoimmune inflammation via IL-21 signalling. PLoS One, 2013,8: e56595. [11] Wang L, Sun Y, Zhang Z, et al. CXCR5+ CD4+ T follicular helper cells participate in the pathogenesis of primary biliary cirrhosis. Hepatology, 2015,61: 627-638. [12] Adam L, Zoldan K, Hofmann M, et al. Follicular T helper cell signatures in primary biliary cholangitis and primary sclerosing cholangitis. Hepatol Commun, 2018,2: 1051-1063. [13] Hou X, Yang Y, Chen J, et al. TCRbeta repertoire of memory T cell reveals potential role for Escherichia coli in the pathogenesis of primary biliary cholangitis. Liver Int, 2019,39: 956-966. [14] Shuai Z, Wang J, Badamagunta M, et al. The fingerprint of antimitochondrial antibodies and the etiology of primary biliary cholangitis. Hepatology, 2017,65: 1670-1682. [15] Pacini G, Carotenuto A, Rentier C, et al. Role of lipoylation of the immunodominant epitope of pyruvate dehydrogenase complex: toward a peptide-based diagnostic assay for primary biliary cirrhosis. J Med Chem, 2015,58: 6619-6629. [16] Migliaccio C. Heterogeneous response of antimitochondrial autoantibodies and bile duct apical staining monoclonal antibodies to pyruvate dehydrogenase complex E2: the molecule versus the mimic. Hepatology, 2001,33: 792-801. [17] Tanaka A, Leung P, Gershwin M E. Evolution of our understanding of PBC. Best Pract Res Clin Gastroenterol, 2018,34-35: 3-9. [18] Sasaki M, Miyakoshi M, Sato Y, et al. Chemokine-Chemokine receptor CCL2-CCR2 and CX3CL1-CX3CR1 axis may play a role in the aggravated inflammation in primary biliary cirrhosis. Digestive Diseases and Sciences, 2014,59: 358-364. [19] Thapa M, Carr DJ. CXCR3 deficiency increases susceptibility to genital herpes simplex virus type 2 infection: Uncoupling of CD8+ T-cell effector function but not migration. J Virol, 2009,83: 9486-9501. [20] Groom JR, Luster AD. CXCR3 in T cell function. Experimental Cell Research, 2011,317: 620-631. [21] Ma HD, Ma WT, Liu QZ, et al. Chemokine receptor CXCR3 deficiency exacerbates murine autoimmune cholangitis by promoting pathogenic CD8(+) T cell activation. J Autoimmun, 2017,78: 19-28. [22] Gorelik L, Flavell RA. Abrogation of TGFbeta signaling in T cells leads to spontaneous T cell differentiation and autoimmune disease. Immunity, 2000,12: 171-181. [23] Gorelik L, Flavell RA. Abrogation of TGFβ signaling in T cells leads to spontaneous T cell differentiation and autoimmune disease. Immunity, 2000,12: 171-181. |