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Immunosuppressive effect of IDO on T cells in patients with chronic hepatitis B*.
Chen, Yong-Bing; Li, Si-Dan; He, Yi-Ping; Shi, Xian-Jie; Chen, Yong; Gong, Jian-Ping.
Afiliação
  • Chen YB; Department of Hepatobiliary Surgery, Chinese PLA General Hospital, Beijing, China.
Hepatol Res ; 39(5): 463-8, 2009 May.
Article em En | MEDLINE | ID: mdl-19207575
ABSTRACT

AIM:

Recently indoleamine 2,3-dioxygenase (IDO) has drawn considerable attention as a mechanism of immune regulation. Our study was to observe the role of IDO in immune tolerance of chronic hepatitis B (CHB), so as to provide a novel approach for reestablishment of active immunity.

METHODS:

Peripheral venous blood samples were taken from 50 CHB patients and HBV viral load, T lymphocyte subsets as well as the mRNA, protein and activity of IDO were detected. The correlations between HBV viral load, T lymphocyte subsets and IDO were statistically analyzed. Blood samples from 50 healthy people were tested as a control group.

RESULTS:

In CHB patients, the mRNA, protein and activity of IDO were all significantly more than those in control group (mRNA[2.11 +/- 0.615] x 10(3) vs. [0.143 +/- 0.026] x 10(3); protein 0.22 +/- 0.06 vs. 0.02 +/- 0.0017; activity 26.07 +/- 8.12 vs. 4.98 +/- 1.65; P < 0.05) and IDO mRNA was positively correlated with HBV viral load (r = 0.502, P < 0.001) and alanine aminotransferase (ALT) (r = 0.65, P < 0.01). Furthermore, IDO mRNA, protein and activity were negatively correlated with CD4(+) T cells (r = -0.622, -0.682, -0.549 respectively, P < 0.05), CD8 (+) T cells (r = -0.487, -367, -294 respectively, P < 0.05) and the ratio of CD4/CD8 (r = -0.426, -0.533, -0.397 respectively, P < 0.05).

CONCLUSION:

IDO closely correlates with HBV viral load and is responsible for immunotolerance against HBV. Suppression of IDO could be a novel approach to break tolerance in CHB.

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2009 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2009 Tipo de documento: Article