Xuebin Qin

My current research originated with an interest in genetics. After participating in the Chinese arm of Human Genome Project, I came to the United States in 1996. Here I began my work on a mouse model of Neuronal Ceroid Lipofuscinosis (NCL), a debilitating, ultimately fatal, human inherited disease that also occurs in mice. In 1998, I joined the Laboratory for Membrane Transport at Harvard Medical School where I have focused on studying the role of complement in the pathogenesis of human diseases using molecularly engineering mouse models.

In the past 10 years, I have generated the several molecularly engineering mouse models. These mouse models are 1) mouse CD59 knockout mice; and 2) human CD59 transgenic mice expressing human CD59 only in the mouse erythrocytes or only in the mouse endothelial and circulating cells. CD59 is a critical complement regulator for restricting complement membrane attack complex (MAC). To define the role of MAC in the pathogenesis of atherosclerosis and aneurysm, I introduced these mouse models to Apoe deficient background. By the utilization of these mice, I have demonstrated the protective role of CD59 in atherosclerosis and aneurysm and established the critical role of MAC in the development of atherosclerosis and aneurysm. I am working on defining the underlying molecular and cellular mechanisms of MAC in the pathogenesis of atherosclerosis and aneurysm.