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Updated: Dec 31, 2025
Author Spotlight: Advancements and Challenges in Hepatitis B Virus Detection
Published on: December 15, 2023
The serum interleukin-26 level is a potential biomarker for chronical hepatitis B
Liwen Luo1, Li Jiang2, Zhiqiang Tian3
1Department of Pathophysiology and High Altitude Pathology.
Insights
Proinflammatory interleukin-26 (IL-26) is elevated in chronic hepatitis B (CHB) patients. Its levels decrease with telbivudine treatment, suggesting IL-26 may be a biomarker for CHB prognosis and treatment effectiveness.
Area of Science:
- Immunology
- Hepatology
- Biomarker Discovery
Background:
- Proinflammatory interleukin-26 (IL-26) is implicated in chronic inflammation.
- The specific role of IL-26 in chronic hepatitis B (CHB) has not been previously established.
Purpose of the Study:
- To investigate the role and potential biomarker value of serum IL-26 in CHB patients.
- To quantify IL-26 levels in CHB patients during telbivudine (LdT) treatment.
Main Methods:
- Serum IL-26 levels were measured in CHB patients at baseline and during LdT treatment.
- Correlations between IL-26, hepatitis B e antigen (HBeAg) seroconversion, HBV DNA, liver enzymes, and T helper 17 (Th17) cell markers were analyzed.
- Expression of IL-26 in CD4 cells and correlation with RORγt mRNA in CHB patients were examined.
Main Results:
- Serum IL-26 was significantly elevated in CHB patients compared to healthy controls.
- IL-26 levels decreased over time during LdT treatment, correlating with HBeAg seroconversion and reduced HBV DNA and liver enzymes.
- IL-26 levels paralleled IL-17 trends, and IL-26 expression was higher in CD4 cells, suggesting Th17 CD4 cells as a potential source.
Conclusions:
- Serum IL-26 is a novel potential biomarker for CHB prognosis and treatment monitoring.
- Elevated IL-26 in CHB may originate from Th17 CD4 cells.
- IL-26 levels dynamically change with antiviral therapy in CHB.
Abstract:
Proinflammatory interleukin-26 (IL-26) is involved in chronic inflammation; however, the role of IL-26 in chronic hepatitis B (CHB) remains unknown.In this study, serum IL-26 was quantified in a cohort of CHB patients at baseline and during telbivudine (LdT) treatment.Our results showed that the serum IL-26 level was significantly elevated in CHB patients compared with that in healthy controls and was time-dependently decreased during LdT treatment, accompanying hepatitis B e antigen (HBeAg) seroconversion and reduced serum levels of hepatitis B virus (HBV) DNA, aspartate transaminase, and alanine transaminase across baseline and treatment. In addition, the serum level of IL-26 exhibited a similar declining trend to that of T helper 17 (Th17) cell-secreted IL-17 during LdT treatment in CHB patients. The percentage of IL-26-expressing CD4 cells was significantly higher than that of IL-26-expressing CD4 cells isolated from the peripheral blood mononuclear cells of CHB patients, suggesting that serum IL-26 might be mainly released from CD4 T cells. Furthermore, the baseline mRNA levels of IL-26 and orphan nuclear receptor RORγt-an important transcription factor expressed by Th17 cells-were positively correlated and displayed the same declining trend across the baseline and LdT treatment in CHB patients, suggesting that Th17 cells could be a possible cellular source of the increased serum IL-26 in CHB patients.Taken together, our results suggest that serum IL-26, possibly produced by Th17 CD4 cells, is a novel and potential biomarker for CHB prognosis and treatment.
