Pathogenic infections result from the failure of the host immune response to prevent the spread or replication of an invading organism. The immune armamentarium includes a wide variety of innate and adaptive elements that are specifically recruited into responses according to the kind and location of the infection. Adaptive immunity provides antigen specificity, and more importantly, memory of a given infection. Adaptive immunity requires the correct development and regulation of T and B lymphocytes. T and B cell development and activity are controlled by a panoply of cell surface receptors that coordinate lymphocyte motility, adhesion, and activation. Our lab seeks to understand the intracellular molecular complexes that integrate the signals transduced from these various receptors. We are currently focused on elements of the actin cytoskeleton as coordinators of signal integration. Actin cytoskeletal elements provide platforms for the assembly of molecular signaling complexes, as well as providing the cellular structure required for the shape changes required for movement and activation. We are working with one specific actin-bundling protein called L-plastin. L-plastin is required for full T cell activation and motility. We are using mice genetically deficient for L-plastin to probe the precise requirements for L-plastin in immune function. Please see our Projects page for details.