Stephen D. Miller, PhD

Stephen D. Miller, PhD, is internationally known for his research on pathogenesis and the regulation of autoimmune diseases and is a coinventor of the COUR tolerogenic immune-modifying particle technology platform. Dr. Miller is the Judy E. Guggenheim Research Professor of Microbiology-Immunology at the Northwestern University

Feinberg School of Medicine in Chicago. He is a consultant to a number of biotechnology and pharmaceutical companies, having assisted in the development of 3 new chemical entities from proof of concept through phase 3 testing. Dr. Miller has served or currently serves on grant review panels for the NIH, the National Multiple Sclerosis Society, the Immune Tolerance Network, and the Juvenile Diabetes Research Foundation and on the editorial boards of multiple journals. He received his PhD in 1975 from Pennsylvania State University and did postdoctoral training at the University of Colorado Health Sciences Center before joining the faculty at Northwestern in 1981.

Dr. Miller’s work has significantly enhanced the understanding of the immune inflammatory processes underlying chronic autoimmune disease, employing animal models of multiple sclerosis (MS) and type 1 diabetes (T1D). He was the first to describe the contribution of epitope spreading to endogenous self-tissue antigens in mediating chronic CNS damage in both autoimmune (experimental autoimmune encephalomyelitis) and Theiler’s virus-induced demyelinating disease models of MS and more recently in T1D in NOD mice. Dr. Miller is also noted for his work describing the cellular and molecular mechanisms underlying the initiation and progression of autoimmunity by infection-induced molecular mimicry. The most widely known aspect of his scientific career is the study of the cellular and molecular mechanisms underlying the treatment of established T-cell–mediated autoimmune diseases using antigen-specific therapies including regulatory T cells, short-term costimulatory molecule blockade strategies, and induction of immune tolerance to autoantigens induced via intravenous injection of apoptotic antigen-pulsed leukocytes and nanoparticles.