David Parker

The Parker laboratory is interested in the cell-surface molecules and intracellular signaling pathways which determine whether an encounter between helper T cells and B cells or other antigen presenting cells results in immunity or tolerance. In a simplified model of peripheral tolerance to self, the Parker lab found that a signal through OX40 (CD134) blocks functional anergy in transferred T cells responding to transgenic or allogeneic antigens, drives the T cells to differentiate into cytokine-secreting effector cells, and results in fatal acute graft versus host disease in unirradiated recipient animals. Current work is focused on the role of the alternative pathway of NFkB activation in that model. In a second project, the lab is exploring the possibility that certain subsets of weakly autoreactive B cells play an essential role as antigen-presenting cells in inducing tolerance to self antigens in T cells. In a third project, the lab is exploring the specific delivery of effector cytokines from T cells to antigen presenting cells, with an emphasis on the membrane-bound TNF family members, CD40L (CD154) and FasL.

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