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Emerg Microbes Infect. 2014 Jul;3(7):e51. doi: 10.1038/emi.2014.51. Epub 2014 Jul 16.

The impact of the interferon-lambda family on the innate and adaptive immune response to viral infections.

Author information

1
Infection Biology, Department of Biomedicine, University Hospital of Basel , 4031 Basel, Switzerland ; Clinical Microbiology, University Hospital of Basel , 4031 Basel, Switzerland.
2
Department of Medical Microbiology and Immunology, and Li Ka Shing Institute of Virology, University of Alberta , Edmonton, Alberta T6G 2E1, Canada.
3
Department of Medical Microbiology and Immunology, and Li Ka Shing Institute of Virology, University of Alberta , Edmonton, Alberta T6G 2E1, Canada ; Division of Infectious Diseases, University of Alberta , Edmonton, Alberta T6G 2E1, Canada.

Abstract

Type-III interferons (IFN-λ, IFNL) are the most recently described family of IFNs. This family of innate cytokines are increasingly being ascribed pivotal roles in host-pathogen interactions. Herein, we will review the accumulating evidence detailing the immune biology of IFNL during viral infection, and the implications of this novel information on means to advance the development of therapies and vaccines against existing and emerging pathogens. IFNLs exert antiviral effects via induction of IFN-stimulated genes. Common single nucleotide polymorphisms (SNPs) in the IFNL3, IFNL4 and the IFNL receptor α-subunit genes have been strongly associated with IFN-α-based treatment of chronic hepatitis C virus infection. The clinical impact of these SNPs may be dependent on the status of viral infection (acute or chronic) and the potential to develop viral resistance. Another important function of IFNLs is macrophage and dendritic cell polarization, which prime helper T-cell activation and proliferation. It has been demonstrated that IFNL increase Th1- and reduce Th2-cytokines. Therefore, can such SNPs affect the IFNL signaling and thereby modulate the Th1/Th2 balance during infection? In turn, this may influence the subsequent priming of cytotoxic T cells versus antibody-secreting B cells, with implications for the breadth and durability of the host response.

KEYWORDS:

B cells; T cells; hepatitis C virus; immune response; innate immunity; interferon-lambda; receptor; respiratory viruses

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