Stephen D. Miller, PHD

Dr. Miller is internationally known for his research on pathogenesis and regulation of autoimmune diseases and is co-inventor of the Cour toleragenic immune modifiying particle technology platform. Dr. Miller is the Judy E. Gugenheim Research Professor of Microbiology-Immunology at 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 three new chemical entities from proof of concept through to Phase 3 testing. He has served or currently serves on grant review panels for the National Institute of Health, the National MS Society, the Immune Tolerance Network and the Juvenile Diabetes Research Foundation and on the editorial boards of multiple journals. He received his Ph.D. in 1975 from the Pennsylvania State University and did postdoctoral training at the University of Colorado Health Sciences Center before joining the faculty at Northwestern in 1981.

His work has significantly enhanced the understanding of 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 (EAE) and Theiler’s virus-induced demyelinating disease models of MS and more recently in T1D in NOD mice. He is also noted for his work describing the cellular and molecular mechanisms underlying initiation and progression of autoimmunity by infection-induced molecular mimicry. The most widely known aspect of Dr. Miller’s scientific career has focused on the study of the cellular and molecular mechanisms underlying treatment of established T cell-mediated autoimmune diseases using antigen-specific therapies – including regulatory T cells (Tregs), short-term co-stimulatory molecule blockade strategies, and induction of immune tolerance to autoantigens induced via i.v. injection of apoptotic antigen-pulsed leukocytes and nanoparticles.