Type I IFN (IFN-I) was firstly described in 1957 as a soluble factor responsible for viral resistance in vitro. Today, it is well known that the IFN-I family comprises a wide number of
cytokines with different modulatory effects on angiogenesis, cell growth,
fibrosis, and apoptosis. However, one of the most important functions of IFN-I is the capability to trigger a complex array of cellular responses that result in a host-protective
antiviral response. For this reason, IFN-I can be considered a "director" of protective immune responses. The recent finding of the so-called
interferon signature in patients suffering from different
autoimmune diseases has underlined its possible role in the pathogenesis of these diseases. On the other hand, IFN-alpha/beta is reported to be efficacious in the treatment of some autoimmune and
infectious diseases not responsive to conventional
therapy. On these occasions, the treated patients often start or increase
autoantibody production supporting the role of IFN as inducer of an autoimmune response. In this review, we will underline recent acquisitions about IFN-I biology, with a focus on the relevance of the induction of some
autoimmune diseases, such as
systemic lupus erythematosus,
systemic sclerosis,
rheumatoid arthritis, dermato/polymiositis, and
Sjogren's syndrome.