Understanding why interferon-beta elicits different functional effects on the immune system from closely related interferon-alpha molecules is described in a report published online this week in Nature Immunology.
Interferons (IFNs) are soluble mediators that influence both innate and adaptive immune responses to microbial infection or tumors. Type I IFN family members include several IFN-alpha and a unique IFN-beta, both of which are recognized by a receptor complex composed of IFNAR2 and IFNAR1 but much of the signaling properties are conferred by the IFNAR2 subunit.
Paul Hertzog and Jamie Rossjohn discover that IFN-beta forms a high-affinity complex with IFNAR1 alone. This interaction triggers a signaling pathway distinct from that induced by the IFNAR2-IFNAR1 complex and leads to activation of a discrete set of genes.
These findings are clinically relevant as IFN-alpha is administered therapeutically to patients with hepatitis virus infections, whereas IFN-beta is used specifically to ameliorate disease symptoms for multiple sclerosis (MS) patients.
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