| The contribution of NF-kappaB signaling to the regulation of protective immunity in Drosophila and humans indicates a role for this pathway as an evolutionarily conserved element in an organism's response to infection (Hoffmann et al., 1999). Thus, NF-kappaB signaling exerts a strong selective pressure on infectious agents, providing a reproductive advantage to organisms that are able to modulate this pathway. The studies presented here address two aspects of the role of NF-kappaB in immunity to the intracellular parasite Toxoplasma gondii. First, they highlighted the activation of NF-kappaB 1 following infection as well as its requirement for resistance to this parasite; second, they revealed an ability of T. gondii to suppress NF-kappaB signaling in the cells that it parasitizes. These observations led to experiments that provided novel insights into the differential role of NF-kappaB1 in cells of differing lineages, and identified the phosphorylation of p65 as a novel target that can be manipulated by T. gondii to promote its survival. Through these studies we have gained an appreciation for the complex roles that NF-kappaB family members play in the regulation of immunity to T. gondii and the intimate relationship between this parasite and the NF-kappaB signaling pathway in infected cells. Understanding the mechanisms utilized by toxoplasma to regulate NF-kappaB signaling will aid in our appreciation of the host-parasite relationship as well as provide insight into the development of the immune response during infection. |
