期刊
JOURNAL OF VIROLOGY
卷 79, 期 23, 页码 14852-14862出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.79.23.14852-14862.2005
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资金
- NIAID NIH HHS [P01 AI48198, R01 AI030798, R01 AI30798, P01 AI048198] Funding Source: Medline
- NIDCR NIH HHS [R01 DE015935] Funding Source: Medline
Infection with high-risk human papillomavirus (HPV) types, particularly types 16 and 18, contributes to 90% of cervical cancer cases. HPV infects cutaneous or mucosal epithelium, tissue that is monitored for microbial infection or damage by Langerhans cells. In lesions produced by HPV type 16, there is a reduction in numbers of immune cells, especially Langerhans cells. Langerhans precursor cells selectively express CCR6, the receptor for macrophage inflammatory protein 3 alpha (MIP-3 alpha), and function as potent immune responders to inflamed epithelium and initiators of the innate immune response. It has been reported that E6 and E7 of high-risk HPVs interfere with immune mediators in order to suppress the recruitment of immune cells and antiviral activities of infected cells. Here we show that, following proinflammatory stimulus, HPV-16 E6 and E7 inhibit MIP-3 alpha transcription, resulting in suppression of the migration of immature Langerhans precursor-like cells. Interestingly, the E6 and E7 proteins from the low-risk HPV types also inhibited MIP-3 alpha transcription. These results suggest that one mechanism by which HPV-infected cells suppress the immune response may be through the inhibition of a vital alert signal, thus contributing to the persistence of HPV infection.
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