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- W2380293489 abstract "To identify the frequency and interferon (IFN)-alpha-producing ability of circulating type 2 pre-dendritic cells (pDC2) and evaluate its role in liver cirrhotic patients with chronic HBV infection.27 liver cirrhotic patients were included in our study and 25 patients with chronic hepatitis B and 25 healthy individuals were enrolled as controls. The numbers of circulating pDC2 and lymphocytes including CD4+ T cells, CD8+ T cells, NK cells as well as B cells were analyzed by flow cytometry. The IFN-alpha-producing function of peripheral blood mononuclear cells (PBMCs) representing the circulating pDC2 was determined by ELISA assay after stimulated by ultraviolet-inactivated herpes simplex virus-1 (UV-HSV-1).The number of pDC2 were (7.21+/-2.38)*10(6)/L, (4.49+/-3.08) *10(6)/L and (2.89+/-1.17) *10(6)/L for healthy control, chronic hepatitis B and cirrhotic patients respectively. Both the number and IFN-alpha-producing function of circulating pDC2 in liver cirrhotic patients significantly lower than that in healthy subjects. There was a correlated simultaneous decrease numbers of circulating CD8+ T cells, NK cells in HBV-infected cirrhotic patients. Furthermore, cirrhotic patients with opportunistic infections have lower numbers of pDC2, CD8+ T cells and NK cells compared to those without opportunistic infections.Liver cirrhotic patients with chronic HBV infection have a significant decrease of circulating pDC2 level and IFN-alpha-producing function. The decreased number and function of pDC2, together with the lower number of CD8+ T cells and NK cells may result in the decline of host immune response, which may partially contribute to the disease progression of HBV infection and opportunistic infections." @default.
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- W2380293489 date "2004-05-01" @default.
- W2380293489 modified "2023-09-25" @default.
- W2380293489 title "[Frequency and function decrease of circulating type 2 pre-dendritic cells (pDC2) and its clinical significance in liver cirrhotic patients with chronic HBV infection]." @default.
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