Age-related macular degeneration
Age-related macular degeneration (AMD) is a disease of the central retina, the macula, and is the most common cause of vision loss in the industrialized world. Although the pathogenesis is largely unknown, it revolves around the atrophy of the retinal pigment epithelium (RPE), the outermost layer of the retina. The RPE plays crucial roles in the homeostasis of the retina, including protecting the photoreceptors responsible for our vision. If RPE cell health is compromised, the photoreceptors and vision are also affected. The retina is an immune-privileged site, and the RPE helps maintain this status through numerous immunoregulatory mechanisms. However, the RPE is also capable of producing many pro-inflammatory factors, and thus can influence the retinal immune status. Aging, oxidative stress, and inflammation have all been implicated in AMD etiology. We investigate the interactions between the immune system and the RPE using in vitro and in vivo techniques, and through the collection of patient samples.
Uveitis is an inflammatory process in the eye which can affect both the iris and retina. Recurrent incidences of uveitis can lead to blindness, and often the specific cause leading to the development of uveitis remains unsolved. We work to define the early events in the pathogenesis of uveitis in order to contribute to the
Beta-2-microglobulin and complement
The protein beta-2-microglobulin is present in free form in all biological fluids as well as on the surface of all nucleated cells as part the major histocompatibility complex class I antigens (MHC). We have discovered that C1 complement can cleave beta-2-microglobulin. The cleaved form of protein has different physiochemical properties, and has been shown to be expressed on the surface of activated cells. The C1 complement mediated cleavage of beta-2-microglobulin might have biological significance linking the innate and adaptive immune system.