Mesalamine-induced B7-H1 expression on hepatic stellate cells attenuates autoimmune liver injury

• Published in: Hepatology research 2011-01, Vol.41 (1), p.79-86
• Main Authors: Lee, Jeong-Hoon, Yoon, Jung-Hwan, Lee, Yu-Jeong, Yang, Jong In, Kwak, Min-Sun, Cho, Eun Ju, Jang, Eun Sun, Yu, Su Jong, Choi, Dae Hee, Jung, Eun Uk, Kim, Hwi Young, Kim, Bo Hyun, Chung, Goh Eun, Kim, Yoon Jun, Jang, Ja-June, Kim, Chung Yong, Lee, Hyo-Suk
• Format: Article
• Language: English
• Subjects: apoptosis; autoimmune hepatitis; B7-H1; concanavalin A; mesalamine
• ISSN: 1386-6346; 1872-034X
• DOI: 10.1111/j.1872-034X.2010.00735.x

Aim:  Hepatic stellate cells (HSCs) have immune regulatory functions. Mesalamine is an effective immune regulatory drug for inflammatory bowel disease. Thus, we hypothesized that mesalamine may also modulate the immune regulatory functions of HSCs. Since B7‐H1 plays a crucial role in regulating T‐cell apoptosis, we evaluated if mesalamine induces B7‐H1 expression on HSCs, and if so, whether mesalamine attenuates autoimmune liver injury in vivo. Methods:  LX‐2 cells, an immortalized human HSC cell line, and human peripheral T‐cells were used in this study. B7‐H1 expression on LX‐2 cells following mesalamine treatment was examined by using flow cytometry. Cell viability was analyzed by MTS assay. Concanavalin‐A (ConA) mice hepatitis model was used for in vivo study. Results:  Flow cytometry showed that mesalamine treatment increased the B7‐H1‐expressing LX‐2 cell fraction from 45.4% to 88.2%, of which increment is equivalent to that of positive control (29.9%, interferon γ‐treated cells). Human T‐cells incubated with LX‐2 cells showed significantly less cell viability in the presence of mesalamine than cells without mesalamine treatment (P