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Published on: October 20, 2021
CD69 Expression is Negatively Associated With T-Cell Immunity and Predicts Antiviral Therapy Response in Chronic
Yurong Gu1, Yanhua Bi2, Zexuan Huang2
1Department of Infectious Diseases, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Insights
CD69 expression on T cells is low in chronic hepatitis B (CHB) and decreases with treatment. Lower CD69 levels predict successful antiviral therapy outcomes in CHB patients.
Area of Science:
- Immunology
- Hepatology
- Virology
Background:
- The role of CD69 on T cells in chronic hepatitis B (CHB) pathogenesis and treatment response is not well understood.
- Investigating CD69's function is crucial for understanding T cell-mediated immunity in CHB.
Purpose of the Study:
- To clarify the function of CD69 expressed on T cells in the context of CHB disease progression.
- To determine the impact of CD69 on T cells during antiviral therapy for CHB.
Main Methods:
- Flow cytometry was used to measure CD69 expression, cytokine production, T-helper cell subsets, and inhibitory molecules on T cells.
- 335 treatment-naive CHB patients and 93 patients on antiviral therapy were analyzed.
- Clinical and virological data were dynamically monitored during antiviral treatment.
Main Results:
- CD69 expression was lowest during the immune-active phase of CHB, inversely correlating with liver damage and inflammatory markers.
- CD69 levels on T cells decreased after 48 weeks of antiviral therapy.
- Lower baseline CD69 expression predicted hepatitis B e antigen (HBeAg) seroconversion, with high accuracy (AUC=0.870).
Conclusions:
- CD69 negatively regulates T cell immunity in CHB and its expression diminishes with antiviral treatment.
- CD69 expression serves as a predictive biomarker for HBeAg seroconversion.
- CD69 may significantly influence T cell regulation and the effectiveness of antiviral therapies in CHB.
Background:
The function of CD69 expressed on T cells in chronic hepatitis B (CHB) remains unclear. We aimed to elucidate the roles of CD69 on T cells in the disease process and in antiviral therapy for CHB.
Methods:
We enrolled 335 treatment-naive patients with CHB and 93 patients with CHB on antiviral therapy. CD69, antiviral cytokine production by T cells, T-helper (Th) cells, and inhibitory molecules of T cells were measured using flow cytometry, and clinical-virological characteristics were examined dynamically during antiviral therapy.
Results:
CD69 expression on CD3+, CD4+, and CD8+ T cells was the lowest in the immune-active phase and was negatively correlated with liver transaminase activity, fibrosis features, inflammatory cytokine production by T cells, and Th-cell frequencies but positively with inhibitory molecules on T cells. CD69 expression on CD3+, CD4+, and CD8+ T cells decreased after 48 weeks of antiviral therapy, and patients with hepatitis B e antigen (HBeAg) seroconversion in week 48 showed lower CD69 expression on T cells at baseline and week 48. The area under the ROC curve of CD69 expression on T cells at baseline for predicting HBeAg seroconversion in week 48 was 0.870, the sensitivity was 0.909, and the specificity was 0.714 (P =0.002).
Conclusions:
CD69 negatively regulates T-cell immunity during CHB, and its expression decreases with antiviral therapy. CD69 expression predicts HBeAg seroconversion in week 48. CD69 may play an important negative role in regulating T cells and affect the efficacy of antiviral therapy.
