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2017 ; 8
(ä): 119
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Interferon Lambda: Modulating Immunity in Infectious Diseases
#MMPMID28293236
Syedbasha M
; Egli A
Front Immunol
2017[]; 8
(ä): 119
PMID28293236
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Interferon lambdas (IFN-?s; IFNL1-4) modulate immunity in the context of
infections and autoimmune diseases, through a network of induced genes. IFN-?s
act by binding to the heterodimeric IFN-? receptor (IFNLR), activating a STAT
phosphorylation-dependent signaling cascade. Thereby hundreds of IFN-stimulated
genes are induced, which modulate various immune functions via complex forward
and feedback loops. When compared to the well-characterized IFN-? signaling
cascade, three important differences have been discovered. First, the IFNLR is
not ubiquitously expressed: in particular, immune cells show significant
variation in the expression levels of and susceptibilities to IFN-?s. Second, the
binding affinities of individual IFN-?s to the IFNLR varies greatly and are
generally lower compared to the binding affinities of IFN-? to its receptor.
Finally, genetic variation in the form of a series of single-nucleotide
polymorphisms (SNPs) linked to genes involved in the IFN-? signaling cascade has
been described and associated with the clinical course and treatment outcomes of
hepatitis B and C virus infection. The clinical impact of IFN-? signaling and the
SNP variations may, however, reach far beyond viral hepatitis. Recent
publications show important roles for IFN-?s in a broad range of viral infections
such as human T-cell leukemia type-1 virus, rotaviruses, and influenza virus.
IFN-? also potentially modulates the course of bacterial colonization and
infections as shown for Staphylococcus aureus and Mycobacterium tuberculosis.
Although the immunological processes involved in controlling viral and bacterial
infections are distinct, IFN-?s may interfere at various levels: as an innate
immune cytokine with direct antiviral effects; or as a modulator of IFN-?-induced
signaling via the suppressor of cytokine signaling 1 and the ubiquitin-specific
peptidase 18 inhibitory feedback loops. In addition, the modulation of adaptive
immune functions via macrophage and dendritic cell polarization, and subsequent
priming, activation, and proliferation of pathogen-specific T- and B-cells may
also be important elements associated with infectious disease outcomes. This
review summarizes the emerging details of the IFN-? immunobiology in the context
of the host immune response and viral and bacterial infections.
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