Thelper cell 1 (Th1)-dependent delayed hypersensitivity reactions are an important part of host defenses against intracellular infections. Yet, more than two centuries after Jenner's successful inoculation against smallpox, we still do not know exactly how to produce safe vaccines that stimulate Th1 immunity. Specialized bone marrow–derived antigen-presenting cells normally are required to initiate all T cell–dependent immune responses (1). However, in order for Th responses to shift to a Th1 phenotype, interleukin (IL)-12 needs to be present at the time of antigen recognition (2). IL-12 drives natural killer (NK) and Th1 cells to generate interferon (IFN)-γ, that subsequently impels macrophages to initiate delayed hypersensitivity reactions. IFN-γ also inhibits the synthesis of IL-4 and IL-5 by Th2 cells (3). In the absence of IL-12 induced IFN-γ production, Th2 responses usually dominate.
But how do particular infectious agents induce IL-12 release? Accumulating evidence indicates that...
