The goal of this project is to study the regulation of dendritic cells (DCs) and immunodeficiency viruses. The year 1997 was very productive in our lab and resulted in a number of publications. We found that human immunodeficiency virus type I (HIV-1), like simian immunodeficiency virus, requires signaling of CD28 or IL-2 receptors in order to replicate in resting T cells and move to the nucleus to form LTR circles, i.e., set up a latent infection. This finding suggests that selective blockade of certain T cell signaling pathways may reduce virus load in HIV-infected individuals. We developed a method and model for isolating and characterizing macaque DCs and found that we can infect macaque DCs in vitro with HIV-2. We have isolated human blood DCs and found that CD4 ligation signals survival in DCs and makes them more effective antigen-presenting cells. We have also defined a set of genes that are induced after CD40 ligation of immature DCs, including the death receptor, TRAIL, and death caspase, caspase-7. A major effort will continue to be the definition of DC signaling pathways and discovery of how they are affected by HIVs. We reported a role for c-myc in B cell receptor induced death. A novel receptor that we helped to discover was given a new CD number, CDw150. Significant effort was spent on the preparation of review articles on DCs and their role in HIV pathogenesis and a chapter on the mechanisms of cellular cooperation to be published in an encyclopedia of immunology.
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