William J. Karpus

Graduate student
Adviser: Robert H. Swanborg
Degree: Ph.D., 1991
Title of thesis: Phenotypic and functional characterization of postrecovery suppressor cells of experimental autoimmune encephalomyelitis

Contact information (as of 12/1/03):

Associate Professor of Pathology and Microbiology-Immunology
Department of Pathology
Northwestern University 
Feinberg School of Medicine
303 E. Chicago Avenue
W127 Ward 3-290
Chicago, IL 60611
Ph: (312) 503-1005
Fax: (312) 503-1217
Work email: w-karpus@northwestern.edu
Home email: NA

Link to Bill at Northwestern

Current activity: I am currently Associate Professor of Pathology as well as Microbiology-Immunology at Northwestern University, Feinberg School of Medicine in Chicago. My laboratory studies the pathogenesis and regulation of autoimmune encephalomyelitis (EAE), an animal model of human multiple sclerosis (MS). Recently we demonstrated that macrophage inflammatory protein-1a (MIP-1 ) directly plays a role in the pathogenesis of acute EAE through chemoattraction of T cells into the CNS, and that monocyte chemotactic protein-1 (MCP-1) plays a role in the pathogenesis of relapsing EAE. We also are investigating the role of other chemokines (RANTES, MIP-1ß, and MIP-2) in the migration of T cells and macrophages to the CNS as well as the effects of chemokines on the intracellular signaling events involved in the regulation of effector cytokine production. Recent results suggest that chemokines act directly on naive T cells and Th0 cells to drive cytokine production toward either a Th1 (inflammatory) or Th2 (regulatory) phenotype. Specifically, MIP-1 potentiates IFN-gamma production and monocyte chemotactic protein-1 (MCP-1) potentiates IL-4 production. Furthermore, MCP-1 appears to downregulate IL-12 expression during tolerance induction, suggesting a role for chemokines in both T helper cell differentiation and regulation. We are examining the molecular mechanisms of these signaling pathways.

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