Tracking antigen-specific CD4+ T cells November 10th (TUE), 11:00 / Auditorium (1F), PBC Marc K. Jenkins Center for Immunology, University of Minnesota Medical School The AIDS epidemic has made it clear that CD4+ helper T lymphocytes play an important role in adaptive immunity to intracellular infections. My laboratory is trying to understand why this is true. Naïve CD4+ T cells are produced in the thymus and then circulate in a quiescent state through the secondary lymphoid organs. As the result of a random gene segment recombination process and positive and negative selection, each naïve CD4+ T cell that comes out of the thymus expresses a unique surface receptor (TCR) capable of binding to a 9 amino acid peptide bound to a major histocompatibility complex II (MHCII) molecule displayed on B cells, dendritic cells, and phagocytes. These ligands are formed as host cells internalize proteins and degrade them into short peptides, which bind to newly synthesized MHCII molecules depending on the presence of critical anchor residues. During primary infection, microbial proteins are subjected to this process. The host’s survival then depends on the few naïve CD4+ T cells that by chance express TCRs capable of binding specifically to microbial peptide-MHCII ligands. Such cells receive TCR signals, divide, and differentiate into B cell- or phagocyte-helping effector cells, which clear the infection via antibodies or phagocytosis. Most of the effector cells then die but some differentiate into long-lived memory cells capable of rapid response during later infections. Many aspects of this process have been documented in vivo with single cell detection methods developed in my laboratory. This will be the topic of my talk. Inquiry: Prof. Charles Surh (Tel. 279-0650) or AIM Administrative Team (Tel.279-8628, E-mail: varsha@ibs.re.kr)