Also, it has been documented that disruption of ATG7-mediated autophagy can evoke the interferon signaling pathway resulting in apoptosis of HCV-infected immortalized human hepatocytes (Shrivastava et al., 2011), and dramatically enhanced infectivity of human papillomavirus in primary human keratinocytes (Griffin et al., 2013).
Thus, it seems that only SPMS patients with superimposed relapses benefit from interferon beta treatment 15– 18. Interferons have not been documented to be effective in primary progressive MS (PPMS) 19.
Increased expression of Th1-associated cytokines such as interferon γ (IFN-γ) and interleukin 12 (IL-12) has been documented in BD patients [ 5, 6].
Similarly, suicidal ideation and attempts have been documented in previously psychiatrically healthy patients with multiple sclerosis (MS) during and after treatment with interferon-β (IFN-β) (25).
Recurrent hepatitis C was documented in 2008 (Metavir score A2F1) and treated with pegylated interferon-α (PEG-IFN-α) and RBV, with a null response.
For example, it has been well documented that most primary and metastatic tumors are infiltrated by immune cells that produce cytokines, cytotoxic mediators, interleukins, interferons, proteases, growth factors, and angiogenic and lymphangiogenic factors, all of which can be co-opted by neoplastic cells to contribute to the progression of cancer and development of metastases [ 1, 2, 7].
It is well known that interferon (IFN) induces antiviral activity.
It is known that interferons (IFN-α, IFN-β, and IFN-γ) induce PD-L1 in tumor cells and the above data suggested that interferon signaling may mediate PD-L1 expression in this system.
The critical role that Type I interferons play in establishing an antiviral state has been well documented over the last several decades, and there is accumulating evidence suggesting that these cytokines are also important in antibacterial defense against intracellular bacterial infections [ 30- 33].
