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Sustained Changes of Treg and Th17 Cells During Interferon-α Therapy in Patients with Chronic Hepatitis B
Hao Feng1,2, Jie Yin2, Ya-Ping Han1
11 Department of Gastroenterology, The First Affiliated Hospital of Nanjing Medical University, First Clinical Medical College of Nanjing Medical University , Nanjing, China .
Chronic hepatitis B (CHB) is a worldwide infectious disease caused by hepatitis B virus (HBV). HBV mainly damages liver cells through immune response. The purpose of this study was to determine whether there were dynamic changes of Treg and Th17 cells and to judge the value of these indicators to antiviral treatment. Twenty-two CHB patients and selected 30 healthy adults were enrolled. Results showed that the expression of Treg (5.72±0.46 vs. 4.42±0.17, p=0.0019) and Th17 (3.94±0.64 vs. 2.66±3.12, p=0.0436) cells was significantly increased in CHB patients, as well as the level of interleukin-17 (IL-17) (16.88±5.37 vs. 8.59±3.31; p=0.004). Then, we monitored longitudinally the impact of the treatment with interferon-α and found that the suppression of viral replication induced by interferon-α resulted in a decrease in Treg, Th17 cells, and IL-17; we also found that the percentage of Treg and Th17 cells went up without clear evidence of clinical autoimmune disease at the end of treatment. Thus, Treg and Th17 cells might play an important role in interferon-α treatment to eliminate HBV. The level of changes may be served to determine the antiviral efficacy of interferon-α therapy.
Chronic hepatitis B (CHB) is a worldwide infectious disease caused by hepatitis B virus (HBV). HBV mainly damages liver cells through immune response. The purpose of this study was to determine whether there were dynamic changes of Treg and Th17 cells and to judge the value of these indicators to antiviral treatment. Twenty-two CHB patients and selected 30 healthy adults were enrolled. Results showed that the expression of Treg (5.72±0.46 vs. 4.42±0.17, p=0.0019) and Th17 (3.94±0.64 vs. 2.66±3.12, p=0.0436) cells was significantly increased in CHB patients, as well as the level of interleukin-17 (IL-17) (16.88±5.37 vs. 8.59±3.31; p=0.004). Then, we monitored longitudinally the impact of the treatment with interferon-α and found that the suppression of viral replication induced by interferon-α resulted in a decrease in Treg, Th17 cells, and IL-17; we also found that the percentage of Treg and Th17 cells went up without clear evidence of clinical autoimmune disease at the end of treatment. Thus, Treg and Th17 cells might play an important role in interferon-α treatment to eliminate HBV. The level of changes may be served to determine the antiviral efficacy of interferon-α therapy.
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