UCLA researchers discover molecular rules that govern autoimmune disorders

UCLA Engineering Bundles with the right DNA spacing can amplify immune response. An international team led by researchers at UCLA’s Henry Samueli School of Engineering and Applied Science and California NanoSystems Institute has identified an unexpectedly general set of rules that determine which molecules can cause the immune system to become vulnerable to the autoimmune disorders lupus and psoriasis. The breakthrough, described in an article published today in the journal Nature Materials, could lead to new ways of treating the disorders. Led by Gerard C. L. Wong, a UCLA professor of bioengineering and chemistry who is affiliated with CNSI, the multidisciplinary team also included Michel Gilliet of Switzerland’s Lausanne University Hospital, and Jure Dobnikar and Daan Frenkel of the University of Cambridge.  Autoimmune diseases strike when the body attacks itself because it fails to distinguish between host tissue and disease-causing agents, or pathogens. Two such disorders are lupus, which can damage the skin, joints and organs, causing rashes, hair loss and fatigue; and psoriasis, which causes rashes, lesions and arthritis, and creates an increased risk for cancer and diabetes. When a healthy person is infected by a virus, viral DNA can activate immune cells via a receptor called TLR9. The receptor triggers the cells to send signaling molecules called interferons to initiate a powerful defensive response. In people with lupus or psoriasis, these cells are activated ...
Source: UCLA Newsroom: Health Sciences - Category: Universities & Medical Training Source Type: news