期刊
TRENDS IN IMMUNOLOGY
卷 31, 期 10, 页码 391-397出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.it.2010.07.004
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类别
资金
- INSERM
- ANRS
- Institut Paoli-Calmettes
- Breast Cancer Research Foundation
- Association pour la Recherche sur le Cancer [4832]
- Comae departemental de Saone et Loire et du Rhone de la Ligue nationale contre le cancer
- Institut National du Cancer
- INCa [ACI-63-04]
- ACT
- Metescape INCa
- Cancerpole Grand Est-DKFZ
- DEMINAP-Lyon Biopole
- EMBO
HIV-1, hepatitis B virus, hepatitis C virus, and human papillomavirus type 16 cause persistent infections that frequently precede cancer development. Virions of these viruses are weak inducers of interferon-alpha and impair Toll-like receptor (TLR)9 function. Loss of TLR9 responsiveness also occurs in tumors without viral etiology such as breast, ovary, and head and neck carcinomas. Recent reports have suggested that viruses and components of the tumor microenviroment interact with regulatory receptors on plasmacytoid dendritic cells (pDCs) to impair TLR7 and TLR9 signaling, and to downregulate TLR9 gene expression. The limited responsiveness of pDCs might contribute to reduced innate immune responses during chronic viral infections and oncogenesis, and represent a target for new therapeutic approaches based on TLR agonists.
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