Clinical Articles
Copyright ©The Author(s) 1996. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Sep 15, 1996; 2(3): 173-175
Published online Sep 15, 1996. doi: 10.3748/wjg.v2.i3.173
Assessment of natural and interleukin-2-induced production of interferon-gamma in patients with liver diseases
Shi-Bao Chen, Xiao-Hui Miao, Ping Du, Qing-Xuan Wu
Shi-Bao Chen, Xiao-Hui Miao, Department of Gastroenterology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China
Ping Du, Qing-Xuan Wu, Department of Microbiology, Second Military Medical University, Shanghai 200433, China
Shi-Bao Chen, Professor of Internal Medicine, advisor of postgraduate for doctorate, having 84 papers published
Author contributions: All authors contributed equally to the work.
Supported by National Science Foundation of China. No.89138970378.
Correspondence to: Dr. Shi-Bao Chen, Professor, Department of Gastroenterology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China
Telephone: +86-21-63275997-361
Received: July 8, 1996
Revised: August 9, 1996
Accepted: August 24, 1996
Published online: September 15, 1996

AIM: To determine whether the production of lower interferon gamma (IFNl) by lymphocytes in patients with liver diseases is due to defects of the lymphocytes themselves or to other cofactors, such as interleukin-2 (IL-2).

METHODS: Peripheral blood mononuclear cells (PBMCs) from patients with various liver diseases were cultured with or without phytohemagglutinin (PHA) and IL-2. The cells were harvested and counted, and the supernatants were tested for IFNl by a sensitive and quantitative ABC-enzyme-linked immunosorbent assay (ELISA).

RESULTS: IFNl was not found in serum samples from patients or normal individuals. However, IFNl was detectable in supernatants of non-induced and induced PBMCs by ABC-ELISA. In non-induced PBMCs (group 1), the content of IFNl in supernatants from control, chronic active hepatitis (CAH), chronic persistent hepatitis (CPH), and hepatocellular carcinoma (HCC) was 8.72/L, 5.03/L, 6.02/L, and 4.91/L, respectively. The production of IFNl in liver disease was significantly decreased compared to control. In PBMCs stimulated with PHA (group 2), the content of IFNl was 22.71/L, 17.12/L, 14.54/L, and 17.63/L, respectively. In PBMCs induced by IL-2 (group 3), the amount of IFNl in supernatant from control (60.67/L) was much larger than those from CAH (21.70/L), CPH (24.00/L), and HCC (19.15/L) (p < 0.01). When comparing the amount of IFNl in group 3 with that in group 1, we found that IFNl production was enhanced by nearly 4-folds in liver diseases and by over 7-fold in control. In contrast, the number of PBMCs, whether from liver diseases or from control, was increased by only approximately 3-fold.

CONCLUSION: The decreased production of IFNl in liver diseases, including HCC, is mainly due to endogenous defects of lymphocytes but may also involve a decrease in stimulating cofactors, such as IL-2.

Keywords: Liver disease, Interleukin-2, Interferon type II