Autoimmune Disease

rheumatoid arthritis research partners

V. Michael Holers, M.D.

University of Colorado Anschutz Medical Campus

Dr. Holers attended Purdue University and then Washington University School of Medicine. Following an internship and residency at Barnes Hospital, he was a Rheumatology Fellow at the University of Colorado, working with Dr. Brian Kotzin, and then a research postdoctoral fellow with John Atkinson at Washington University. After being appointed as Associate Professor at Washington University, he was recruited in 1993 to the University of Colorado to be the first Smyth Professor of Rheumatology. In 2000, Dr. Holers became Division Head of Rheumatology at the same institution and is currently Professor of Medicine and Immunology and the Scoville Professor of Rheumatology. The historical focus of the Holers Laboratory research efforts has been on the structure-function relationships and biologic roles of the complement system of the immune system, wherein he performed studies which led to the definition of key structure-function relationships, the development of molecular genetic tools, and understanding of the key in vivo roles of these proteins in the pathogenesis of murine models of human disease. The Holers Laboratory also co-developed and then commercialized the first injured tissue-directed complement therapeutics. More recently, Dr. Holers has moved a major focus of research activities to studying the natural history and pathogenesis of human rheumatoid arthritis (RA) prior to and immediately after the onset of clinically apparent arthritis, and paired that with mechanism-based murine studies. To advance this research area, he co-founded the SERA (Studies of the Etiology of Rheumatoid Arthritis) study, which is focused on mechanism-based and epidemiologic assessments of high-risk subject populations. These studies, in collaboration with Dr. Kevin Deane and others, have provided strong evidence for a mucosal origin of RA-related autoimmunity prior to the development of clinically apparent arthritis and identified several candidate immune processes as therapeutic targets.