title: Increased IL-23 and IL-17 expression by peripheral blood cells of patients with primary biliary cirrhosis.
abstract: Primary biliary cirrhosis (PBC) is a typical autoimmune disease for which the pathogenesis remains unclear. IL-23 and IL-17 are pro-inflammatory cytokines of the "IL-23/IL-17 axis," which may play a key role in the pathogenesis of autoimmune diseases. In this study, we investigated the expression of IL-23 and IL-17 in the peripheral blood of patients with PBC and its clinical significance. We used quantitative PCR to determine mRNA expressions of IL-23, IL-23 receptor, and IL-17 in peripheral blood mononuclear cells (PBMC) from PBC patients. ELISA's were used to determine patients' serum levels of IL-23 and IL-17. IL-23- and IL-17-producing cells in liver biopsis were also analyzed. Compared to a healthy control group, the mRNA expression levels of IL-23 p19, its corresponding receptor, IL-23R, and IL-17 in PBMC's from PBC patients were significantly increased, and these levels were correlated with PBC disease stages. PBC patients' serum levels of IL-23 and IL-17 were higher than those in a post-hepatic cirrhosis group and a healthy group, and were significantly higher in the early PBC disease stages than in the advanced PBC stages. There were significantly more IL23+ and IL-17+ mononuclear cells in portal areas of liver tissues in advanced stages of this disease than in the early stages. The serum levels of IL-23 and IL-17 in PBC patients were positively correlated with serum GGT levels. Thus, IL-23 and IL-17 may play an important role in the pathogenesis of PBC by promoting inflammation. Because the IL-23 and IL-17 levels in the peripheral blood of PBC patients were increased and were correlated with clinical stages, they may be indices that could be used to clinically monitor PBC.
authors.affiliation: Department of Laboratory Medicine, 100th Military Hospital, Suzhou 215007, China.
authors.forename: Cheng
authors.initials: C
authors.lastname: Qian
authors.forename: Tingwang
authors.initials: T
authors.lastname: Jiang
authors.forename: Weiwei
authors.initials: W
authors.lastname: Zhang
authors.forename: Chuanlu
authors.initials: C
authors.lastname: Ren
authors.forename: Qianqian
authors.initials: Q
authors.lastname: Wang
authors.forename: Qin
authors.initials: Q
authors.lastname: Qin
authors.forename: Jie
authors.initials: J
authors.lastname: Chen
authors.forename: Anmei
authors.initials: A
authors.lastname: Deng
authors.forename: Renqian
authors.initials: R
authors.lastname: Zhong
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D005260:Female; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D020381:Interleukin-17 / Q000096:biosynthesis / Q000097:blood* / Q000235:genetics; D053759:Interleukin-23 / Q000096:biosynthesis / Q000097:blood* / Q000235:genetics; D053760:Interleukin-23 Subunit p19 / Q000235:genetics; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D008105:Liver Cirrhosis, Biliary / Q000097:blood* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D012333:RNA, Messenger / Q000378:metabolism; D018123:Receptors, Interleukin / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism*; D053707:Receptors, Interleukin-12 / Q000235:genetics; D055815:Young Adult; D005723:gamma-Glutamyltransferase / Q000378:metabolism*
chemical_list: D015415:Biomarkers; C508438:IL12RB1 protein, human; C515500:IL23R protein, human; D020381:Interleukin-17; D053759:Interleukin-23; D053760:Interleukin-23 Subunit p19; D012333:RNA, Messenger; D018123:Receptors, Interleukin; D053707:Receptors, Interleukin-12; D005723:gamma-Glutamyltransferase; C554782:gamma-glutamyltransferase, human
keywords: IL-17; IL-23; Primary biliary cirrhosis (PBC)