Christopher Wilson, M.D. Professor of Immunology and Pediatrics Research Affiliate, Center on Human Development and Disability cbwilson@u.washington.edu 206-685-3956 University of Washington, Box 357650 Seattle, WA 98195-7650

Perinatal infection is a major cause of neurologic injury and long-term disability. Dr. Wilson's research focuses on understanding the cellular and molecular basis for newborns' susceptibility to infection by intracellular bacterial and viral pathogens, which can have significant neurologic consequences. Control of such infections depends on the ability of the innate immune response to limit microbial replication and injury in the initial days of infection, whereas eradication of active infection and resolution of disease depends on the timely development of antigen-specific interferon-γ (IFN- γ)–producing Th1-type CD4 and CD8 T cells.

Wilson’s work addresses the molecular and cellular basis for delayed development of antigen-specific T cell responses in neonates and young infants and for the diminished ability of their T cells to establish and maintain Th1-type T cell responses. One aspect of his current focus of interest is toll-like receptors (TLRs). In addition to their important role in activating innate defenses, TLRs play a critical role in the activation of dendritic cells, which link innate and adaptive immunity, influencing the quality and magnitude of the ensuing antigen-specific T cell response and the outcome of the infection. A second area of work addresses the role of epigenetic processes (DNA methylation and the molecular interplay among DNA methylation, post-translational histone modification, chromatin structure, and lineage-restricted transcription factors) in the commitment of T cells to Th1-type effector programs. As part of these studies, Wilson’s lab is delineating distal regulatory elements in the IFN-γ/Th1 cytokine gene locus to gain a more comprehensive understanding of how Th1-type lineage commitment is controlled. The long-term goal of these studies is to understand the basis for limitations in the ability of neonates and infants to initiate and sustain protective Th1-type responses.

CHDD Outlook article on preventing infections, protecting the developing brain
(Spring 2006, page 1)

Chris Wilson's web page

University of Washington • Center on Human Development and Disability Box 357920 • Seattle WA 98195-7920 USA • 206-543-7701 • chdd@u.washington.edu

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