Journal
CRITICAL REVIEWS IN IMMUNOLOGY
Volume 28, Issue 1, Pages 61-94Publisher
BEGELL HOUSE INC
DOI: 10.1615/CritRevImmunol.v28.i1.40
Keywords
innate immunity; toll-like receptors; RNA helicases; IFN receptor; hepatitis; HIV
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Funding
- NIAAA NIH HHS [AA 14372] Funding Source: Medline
- NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM [R01AA014372, R37AA014372] Funding Source: NIH RePORTER
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Viral infections represent a major source of acute and chronic human disease. The immune system plays a central role in the elimination of viruses through its ability to recognize pathogens and to induce virus-specific cellular activation, accompanied by a robust production of soluble molecules with antiviral effects. Interferons are among the most powerful natural soluble antiviral molecules. Upon viral infection, interferons are produced by a variety of cell types, with immune cells being the main contributors. The immune system works as a well-orchestrated team composed of multiple cell types. The mechanisms of intercellular cooperation that includes dendritic cells (DCs), their soluble factors, and different types of immune cells are yet to be fully understood. Further, the effects of viral infections on interimmune cooperation need to be investigated. In this review, we define the role of plasmacytoid dendritic cells (PDC) and PDC-derived interferon alpha (IFN alpha) during viral infections. Specifically, we address the mechanisms of IFN alpha induction and the cooperation between PDC, PDC-derived IFN(x and T cells, B cells, NK, iNKT, and myeloid dendric cells in antiviral immune responses.
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