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Dr. Clark's laboratory is interested in how B lymphocytes are activated to survive, proliferate or undergo programmed cell death. B cells are very social cells, and their behavior is influenced not only by various forms of specific antigen, but also by receptor-ligand interactions with T lymphocytes (e.g., CD40 ligand), dendritic cells (DCs) and macrophages (e.g., BAFF). A major goal of the laboratory is to define key signaling pathways regulating the fate of B cells after they are activated through antigen, CD40 or BAFF receptors. Recently the lab has focused on extrafollicular antibody responses triggered by pathogens and via DC-controlled processes.
Dr. Clark's laboratory also investigates new methods for delivering antigens into the immune system to either induce protective humoral immunity or turn off humoral immune responses to autoantigens or allergens. DCs are sentinels within the immune system, which respond to pathogens through pattern recognition receptors such as Toll-like receptors (TLR) or C-type lectin receptors (CLRs). These receptors program DCs to migrate to lymph nodes and instruct T cells and B cells to make appropriate responses to infections. Dr. Clark's lab targets antigens to DC subsets or B cells through CLRs or other receptors. A current project is to define how targeting to the TLR family member, CD180, induces protective immunity after West Nile virus infection.
Copyright © 2003-2014 Molecular & Cellular Biology Program, University of Washington
Fred Hutchison Cancer Research Center | University of Washington
Institute for Systems Biology | Seattle Biomed