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Production in Human Peripheral Blood Mononuclear and NK Cells1
*
Laboratory of Cellular Biology, Korea Research Institute of Bioscience and Biotechnology, Taejon, Korea;
Department of Microbiology, College of Medicine, Soonchunhyang University, Chungnam, Korea,
Korean Food and Drug Administration, Seoul, Korea;
Department of Internal Medicine 1, Kurume University School of Medicine, Fukuoka, Japan; and
¶ University of Colorado Health Sciences Center, Denver, CO 80262
Cervical carcinoma is the predominant cancer among malignancies in
women throughout the world, and human papillomavirus (HPV) 16 is the
most common agent linked to human cervical carcinoma. The present study
was performed to investigate the mechanisms of immune escape in
HPV-induced cervical cancer cells. The presence of HPV oncoproteins E6
and E7 in the extracellular fluids of HPV-containing cervical cancer
cell lines SiHa and CaSki was demonstrated by ELISA. The effect of HPV
16 oncoproteins E6 and E7 on the production of IFN-
by IL-18 was
assessed. E6 and E7 proteins reduced IL-18-induced IFN- production
in both primary PBMCs and the NK0 cell line. FACS analysis revealed
that the viral oncoproteins reduced the binding of IL-18 to its
cellular surface receptors on NK0 cells, whereas there was no effect of
oncoproteins on IL-1 binding to its surface IL-1 receptors on D10S, a
subclone of the murine Th cell D10.G4.1. In vitro pull-down assays also
revealed that the viral oncoproteins and IL-18 bound to IL-18R
-chain competitively. These results suggest that the extracellular
HPV 16 E6 and E7 proteins may inhibit IL-18-induced IFN- production
locally in HPV lesions through inhibition of IL-18 binding to its
-chain receptor. Down-modulation of IL-18-induced immune responses
by HPV oncoproteins may contribute to viral pathogenesis or
carcinogenesis.
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