Interferon and Apoptosis in Systemic Lupus Erythematosus

Abstract

Systemic lupus erythematosus (SLE) is generally diagnosed long after the disease begins. This means that the cause of the disease is hard to find, buried in the past. In the search for the elusive causal agents for SLE, one candidate is the immune signaling molecule, interferon (IFN). Interferon is a secreted signaling protein, or cytokine, which is expressed at higher levels in SLE patients and has been associated with incidence and severity of the disease. A combination of environmental triggers and genetic susceptibility combine to initiate SLE. Although there are many etiological components, they usually converge on a heightened state of activation for the immune system, with resultant increases in interferon production and interferon signaling. That is to say that interferon could be thought of as either a causative agent, a result of the disease, or both. This chapter will discuss the basics of interferon function and how de-regulation of apoptosis can lead to interferon production due to immune complexes. We will then discuss how the functioning of the immune system changes in someone with SLE, the genes which are associated with risk for SLE, and clinical manifestations of interferon in SLE.