Molecular Mechanisms Governing Differential Type I Interferons Signaling [Cell Biology]

Type I interferons (IFN-I) are cytokines that affect the expression of thousands of genes, resulting in profound cellular changes. IFN-I activates the cell by dimerizing its two-receptor chains, IFNAR1 and IFNAR2, which are expressed on all nucleated cells. Despite a similar mode of binding, the different IFN-Is activate a variety of outcomes. The causes for differential activation may stem from differences in IFN-I binding affinity, duration of binding, number of surface receptors, induction of feedback loops and cell-type specific variations. All together these will alter the signal that is transmitted from the extracellular domain inwards. The intracellular domains binds directly or indirectly to many different effector proteins that transmit signals. The composition of effector molecules deviate between different cell types and tissues, providing an additional level of complexity to the system. Moreover, IFN-Is do not act on their own, and clearly there is much cross talk between the activated effector molecules by IFN-I and other cytokines. The outcome generated by all of these factors (processing step) is an observed phenotype, which can be cell transformation, initiation of an antiviral state, induction of senescence or apoptosis and many more. In this review I summarize the current knowledge on the mode of activation and processing that is initiated by IFN-I, in perspective of the resulting phenotypes.

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