Abstract
A characteristic feature of hepatitis C virus (HCV) infection is a high frequency of persistence and the progression to chronic liver diseases. Recent data suggest that prevalent T helper (Th) 2 immunity as well as weak HCV-specific T-cell response is associated with viral persistence. Here, we showed that the production of interleukin 12 (IL-12) and nitric oxide (NO) that is critical for the induction of Th1 and innate immunity, but not that of tumor necrosis factor α (TNF-α), was significantly suppressed in both HCV core-expressing macrophage cell lines and mouse peritoneal macrophages treated with recombinant core protein. In addition, IL-12 p40 promoter activity was repressed by the presence of HCV core in macrophages stimulated with lipopolysaccharride (LPS) following IFN-γ treatment, indicating that IL-12 production may be downregulated at the transcriptional level. We also found that proliferation of T cells and IFN-γ, production in mixed lymphocyte reactions (MLR) with core-expressing cells were inhibited. Taken together, our results suggest that HCV core protein could play roles in suppressing the induction of Th1 immunity through inhibition of IL-12 and NO production.
| Original language | English |
|---|---|
| Pages (from-to) | 271-279 |
| Number of pages | 9 |
| Journal | Virology |
| Volume | 279 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 2001 Jan 20 |
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All Science Journal Classification (ASJC) codes
- Virology
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Hepatitis C virus core protein inhibits interleukin 12 and nitric oxide production from activated macrophages. / Lee, Chu Hee; Choi, Yo Han; Yang, Se Hwan; Lee, Chang Woo; Ha, Sang-Jun; Sung, Young Chul.
In: Virology, Vol. 279, No. 1, 20.01.2001, p. 271-279.Research output: Contribution to journal › Article
TY - JOUR
T1 - Hepatitis C virus core protein inhibits interleukin 12 and nitric oxide production from activated macrophages
AU - Lee, Chu Hee
AU - Choi, Yo Han
AU - Yang, Se Hwan
AU - Lee, Chang Woo
AU - Ha, Sang-Jun
AU - Sung, Young Chul
PY - 2001/1/20
Y1 - 2001/1/20
N2 - A characteristic feature of hepatitis C virus (HCV) infection is a high frequency of persistence and the progression to chronic liver diseases. Recent data suggest that prevalent T helper (Th) 2 immunity as well as weak HCV-specific T-cell response is associated with viral persistence. Here, we showed that the production of interleukin 12 (IL-12) and nitric oxide (NO) that is critical for the induction of Th1 and innate immunity, but not that of tumor necrosis factor α (TNF-α), was significantly suppressed in both HCV core-expressing macrophage cell lines and mouse peritoneal macrophages treated with recombinant core protein. In addition, IL-12 p40 promoter activity was repressed by the presence of HCV core in macrophages stimulated with lipopolysaccharride (LPS) following IFN-γ treatment, indicating that IL-12 production may be downregulated at the transcriptional level. We also found that proliferation of T cells and IFN-γ, production in mixed lymphocyte reactions (MLR) with core-expressing cells were inhibited. Taken together, our results suggest that HCV core protein could play roles in suppressing the induction of Th1 immunity through inhibition of IL-12 and NO production.
AB - A characteristic feature of hepatitis C virus (HCV) infection is a high frequency of persistence and the progression to chronic liver diseases. Recent data suggest that prevalent T helper (Th) 2 immunity as well as weak HCV-specific T-cell response is associated with viral persistence. Here, we showed that the production of interleukin 12 (IL-12) and nitric oxide (NO) that is critical for the induction of Th1 and innate immunity, but not that of tumor necrosis factor α (TNF-α), was significantly suppressed in both HCV core-expressing macrophage cell lines and mouse peritoneal macrophages treated with recombinant core protein. In addition, IL-12 p40 promoter activity was repressed by the presence of HCV core in macrophages stimulated with lipopolysaccharride (LPS) following IFN-γ treatment, indicating that IL-12 production may be downregulated at the transcriptional level. We also found that proliferation of T cells and IFN-γ, production in mixed lymphocyte reactions (MLR) with core-expressing cells were inhibited. Taken together, our results suggest that HCV core protein could play roles in suppressing the induction of Th1 immunity through inhibition of IL-12 and NO production.
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UR - http://www.scopus.com/inward/citedby.url?scp=0035916008&partnerID=8YFLogxK
U2 - 10.1006/viro.2000.0694
DO - 10.1006/viro.2000.0694
M3 - Article
C2 - 11145908
AN - SCOPUS:0035916008
VL - 279
SP - 271
EP - 279
JO - Virology
JF - Virology
SN - 0042-6822
IS - 1
ER -