[5][6] IFNs were originally discovered as molecules that could reduce the ability of a normal virus to infect cells, a process called viral 'interference'.

[11] The human IFNA gene family shares 70-80% amino acid sequence homology, and about 35% identity with IFNB.

[17] Viruses and immune complexes (ICs) containing nucleic acids can access intracellular TLRs (TLR3, TLR7/8 and TLR9) after binding to Fc receptors and induce IFN-α production by activation of the IRFs.

[20] Emerging evidence suggests that abnormal IFN production contributes to immune dysfunction and mediates tissue inflammation and organ damage in a number of autoimmune diseases such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), idiopathic inflammatory myopathies (IIM), Sjogren's syndrome (SS) and multiple sclerosis (MS).

Patients with dermatomyositis and polymyositis have increased IFN serum levels which in some studies correlate with disease activity or myositis-specific autoantibodies.

[28][29][30][31] Also, studies have suggested a genetic or heritable component to the high type I IFN observed in myositis patients, similar to SLE.

[32][33] Multiple sclerosis (MS) is a disorder of the central nervous system characterized by inflammation, demyelination and neurodegeneration with presumed autoimmune origin.

Whereas type I IFNs are thought to induce some autoimmune conditions such as SLE as noted above, MS is effectively treated by administering recombinant human IFN-β.

[38] Another phase I clinical trial has reported a dose-dependent inhibition of IFN-α/β-inducible genes in both peripheral blood and skin biopsies in SLE patients treated with anti-IFN monoclonal antibody therapy.