Patients suffering from rheumatoid arthritis and lupus often develop cardiovascular disease at much younger ages than healthy people. This could be due in part to a dysfunctional form of HDL (the “good cholesterol” responsible for preventing inflammation and clogged arteries) present in almost half of lupus patients and one quarter of RA patients, but generally absent from people without autoimmune diseases (< 5%). We do not understand how this dysfunctional, pro-inflammatory HDL (piHDL) promotes cardiovascular disease in RA and lupus, but we do know that piHDL activates monocytes, the main immune cell involved in forming the plaque that clogs arteries. Recent experiments suggest piHDL might differ from normal HDL in composition. Dr. Skaggs will examine piHDL isolated from RA and lupus patients for similarities and differences compared to each other as well as to piHDL isolated from healthy controls. Results from these studies may pinpoint abnormal levels of HDL and proteins in the body that could be targeted to reverse the effects of piHDL and block piHDL-mediated accelerated cardiovascular disease in RA and lupus.