Introduction

Interferon alpha (IFN-α) was one of the first FDA-approved biotherapeutic treatments. Since its approval, it has proved to be a powerful cytokine with potent therapeutic activity but, unfortunately, strong side effects. The overall use of IFN-α increased dramatically when it was approved as the treatment of choice for hepatitis C. However, nearly half of the individuals infected with genotype 1 of the virus still fail to respond to therapy (1). Consequently, several pharmaceutical companies are now trying to turn on the body’s own interferon alpha family of proteins using immunomodulatory molecules in the hope that this will elicit a more complete antiviral response. Both therapeutic approaches are not without risk, due to the side effects associated with IFN-α. Additionally, there is a growing amount of published scientific articles suggesting that IFN-α may be involved in certain autoimmune diseases, including systemic lupus erythematosus (SLE) (2). 

Combined, these observations clearly suggest an increased need to monitor IFN-α levels in both normal and diseased individuals along with patients undergoing therapy. How much IFN-α produced by the body in response to new immunomodulatory therapies will be functionally equivalent to the current IFN-α exogenous treatment regimen? How much ‘basal’ IFN-α is beneficial to prevent or limit viral infection and how much is too much, thereby predisposing an individual to autoimmune disorders? Although IFN-α has been studied for over 50 years, we are only now beginning to understand that interferon can have vastly dichotomous activities. This article will highlight the primary methods currently employed to study interferon levels in research and in clinical settings of this very useful, yet only moderately understood cytokine.

For research use only, not for diagnostic or therapeutic use.