William J. Karpus


Professor, Dean of the Graduate School



217 Bascom Hall
500 Lincoln Dr.
Madison, WI 53706

217 Bascom Hall

Research Interests

I have been studying the role of chemokines in experimental autoimmune encephalomyelitis (EAE) as a model for multiple sclerosis (MS) for 21 years and have been using rat and mouse models of MS to understand demyelinating disease pathogenesis for the past 29 years. We have identified key chemokines and receptors in the regulation of T cell and macrophage migration and function using a variety of approaches including neutralizing antibody treatment and mice deficient for select chemokine ligands or receptors. These studies have identified significant roles for a subset of chemokines and chemokine receptors in EAE pathogenesis and point to these factors as potential therapeutic targets for MS. More recently, we have observed a role for Delta Like Ligand-mediated Notch signaling in the regulation of chemokine receptor cell surface expression in the control of T cell migration to the central nervous system (CNS). Additionally, we have considerable experience investigating mechanisms of immunologic tolerance in CNS demyelinating diseases as an approach for antigen-specific therapy. The current project will determine mechanisms of chemokine regulation that control lymphocyte entry into the brain and identify new drug targets for relapsing MS therapy.

Selected Publications
  • Sugiura Y, Kamdar K, Khakpour S, Young G, Karpus WJ, R DePaolo W.TLR1-induced chemokine production is critical for mucosal immunity against Yersinia enterocolitica.Mucosal Immunol. 2013;6(6):1101-9.
  • Reynolds ND, Lukacs NW, Long N, Karpus WJ. “Delta-like ligand 4 regulates central nervous system T cell accumulation during experimental autoimmune encephalomyelitis.J. Immunol.. 2011;187(5):2803-13.
  • Forde EA, Dogan R-NE, Karpus WJ. “CCR4 contributes to the pathogenesis of experimental autoimmune encephalomyelitis by regulating inflammatory macrophage function.J. Neuroimmunol.. 2011;236(1-2):17-26.