Typically, inflammatory responses in the human body are caused as a result of bacterial or viral infection. However, in chronic conditions like AMD, a form of "sterile" inflammation has recently been described whereby localized immune responses can occur in distinct organs and tissues of the body. This localized response culminates in the activation of a protein complex termed the "inflammasome" which mediates the secretion of two highly inflammatory cytokine proteins, called IL-1beta and IL-18.

Dr. Humphries’ and Dr. Campbell’s team has recently discovered that a component of the inflammasome, IL-18, appears to play a protective role in the development of wet AMD by preventing the expression of VEGF, a key protein involved in the development of choroidal neovascularization (CNV; the damaging ingrowth of blood vessels into the retina). The team discovered that mice lacking the component IL-18 developed exacerbated CNV, which directly implies that this molecule is central to the development of the disease. Current antibody-based therapies in use for treating wet AMD involve the direct intraocular injection of medication targeting VEGF. The team has discovered that IL-18 can actually decrease VEGF levels itself which, while leading to a better understanding of the disease process, could also lead to a new therapeutic strategy for wet AMD. In the future, drugs directed against the inflammasome, including IL-18, will be tested to see if they can reduce the drusen deposits in the retina.