Premium
Human plasmacytoid dendritic cells from patients with chronic hepatitis B virus infection induce the generation of a higher proportion of CD4 + and CD25 + regulatory T cells compared with healthy patients
Author(s) -
Hong Jun,
Gong Zuo Jiong
Publication year - 2008
Publication title -
hepatology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.123
H-Index - 75
eISSN - 1872-034X
pISSN - 1386-6346
DOI - 10.1111/j.1872-034x.2007.00279.x
Subject(s) - il 2 receptor , immunology , cytotoxic t cell , hepatitis b virus , flow cytometry , antigen , biology , t lymphocyte , medicine , virology , t cell , immune system , virus , in vitro , biochemistry
This study was undertaken to investigate whether plasmacytoid dendritic cells (PDC) are involved in the generation of a higher proportion of CD4 + and CD25 + regulatory T (Treg) cells in chronic hepatitis B virus (HBV) infection compared with healthy patients. The amount, phenotype, and function of Treg cells in CD4 + T cells primed by PDC from 46 chronic HBV patients, 25 healthy controls, and 10 individuals with resolved HBV infection were studied by flow cytometry, reverse transcription polymerase chain reaction, enzyme‐linked immunosorbent assay, and proliferation assay. CD4 + T cells primed by PDC from chronic HBV patients were more effective than CD4 + T cells primed by PDC from the healthy controls and the resolved HBV patients in suppressing the hepatitis B core antigen‐specific proliferation and the interferon production. The interleukin‐10 and transforming growth factor‐β1 could also be detected in the supernatants of the PDC‐primed CD4 + T cells. A higher percentage of Treg cells, defined as CD4,CD25, CD45RO, and cytotoxic T‐lymphocyte‐associated antigen 4‐positive cells, was detected within the population of CD4 + T cells primed by PDC from chronic HBV patients compared with the healthy controls and individuals with resolved HBV infection. Accordingly, CD25 + Treg cells from PDC‐primed CD4 + T cells displayed a high Fox P3 messenger RNA level. Depleting CD4 + and CD25 + Treg cells from CD4 + T cells primed by PDC from the chronic HBV patients, the healthy volunteers, and the resolved HBV patients made PDC‐primed CD4 + T lose the capability in suppressing HBV‐specific T cells. PDC from the patients with chronic HBV infection induced the generation of a higher proportion of CD4 + and CD25 + Treg cells compared with the healthy patients.