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[Association between CD4+CD25+Foxp3+ regulatory T cells and serum transforming growth factor beta 1 in patients with

Gui-lin Yang1, Liu-mei Xu, Hong-yan Yao

  • 1The Third People's Hospital of Shenzhen, Shenzhen Guangdong 518020, China.

Zhonghua Gan Zang Bing Za Zhi = Zhonghua Ganzangbing Zazhi = Chinese Journal of Hepatology
|December 5, 2009
PubMed

Insights

Regulatory T cells (CD4+CD25+Foxp3+) and TGF-beta 1 are elevated in chronic hepatitis B (CHB) and asymptomatic carriers (AsC). Their levels correlate with viral load, suggesting a role in maintaining HBV chronicity.

Area of Science:

  • Immunology
  • Hepatology
  • Virology

Background:

  • Hepatitis B virus (HBV) infection can lead to chronic disease.
  • Regulatory T cells (Tregs) play a role in immune suppression.
  • Transforming growth factor beta 1 (TGF-β1) is an immunosuppressive cytokine.

Purpose of the Study:

  • To investigate the association between CD4+CD25+Foxp3+ regulatory T cells and serum TGF-β1 in patients with hepatitis B.
  • To explore the role of these cells and cytokine in the chronicity of HBV infection.

Main Methods:

  • Flow cytometry was used to quantify CD4+CD25+Foxp3+ T cells.
  • Real-time PCR assessed Foxp3 gene expression.
  • ELISA measured serum TGF-β1 levels.
  • Study included patients with chronic hepatitis B (CHB), asymptomatic carriers (AsC), normal subjects (NS), and resolved HBV infection.

Main Results:

  • CHB and AsC patients showed significantly higher frequencies of CD4+CD25+Foxp3+ T cells compared to controls.
  • Foxp3 mRNA levels were elevated in CD4+CD25+ T cells from CHB and AsC patients.
  • The frequency of CD4+CD25+Foxp3+ Tregs correlated with HBV DNA levels in CHB and AsC patients.
  • Serum TGF-β1 levels were increased in CHB and AsC patients and correlated with Foxp3 mRNA expression and Treg frequency.

Conclusions:

  • Aberrant CD4+CD25+Foxp3+ regulatory T cells and elevated serum TGF-β1 are associated with chronic hepatitis B.
  • These findings suggest a mechanism involving Tregs and TGF-β1 in maintaining HBV chronicity.
Abstract

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