The glomerular epithelial cell has a complex shape with foot-like extensions that wrap around capillaries of the glomerulus, forming spaces for the flow of blood filtrate that are called slit diaphragms. In the mice lacking CD2AP, the epithelial cells were damaged and the slit diaphragms were lost. The mice, developed by Shih and Li, died of kidney failure by the time they were six weeks old. To address this question, Shaw revisited a model concerning CD2AP's potential role in T cells of the immune system. He developed this model with colleagues Mike L. Dustin, associate professor of pathology, and Paul M. Allen, Ph.D., the Robert L. Kroc Professor of Pathology.
T cells defend the body from microbes by interacting with another immune system cell.
Shaw previously showed that CD2AP plays an important role in organizing the T cell surface, helping the cell form a molecular bridge with other immune cells. The molecular bridge forms as a T cell molecule binds to another molecule on the other cell. CD2AP helps position the molecule, CD2, and anchor it at the right place in the membrane. CD2 also serves as a border guard, keeping proteins in separate regions on the T cell surface. Shaw and his group were struck by the similarities between CD2 and a recently identified protein called nephrin, which is expressed in glomerular epithelial cells.