ABOVE: © shutterstock.com, mopic
When immunologist Rachel Caspi began studying an inflammatory eye disease called autoimmune uveitis in the mid-1980s, she had to inoculate mice with a protein found in the mammalian retina to spark the disease. Injecting interphotoreceptor retinoid-binding protein (IRBP) along with an immune-stimulating compound called an adjuvant into the animals’ bloodstream prompted the mice’s own T cells to attack their eyes. That led to inflammation, tissue damage, and eventual blindness.
Caspi wanted to work with a model that better represented human uveitis, in which IRBP-specific T cells attack the retina spontaneously, without the need for any sort of exogenous immune stimulation. Ten years ago, she and her team at the National Eye Institute in Bethesda, Maryland, developed a genetic mouse model of the disease in which mice produced artificially large numbers of T cells that bound to IRBP. As in humans, these T cells traveled to the ...
