Bill F. Hawse, PhD

T cells are mediators of the adaptive immune response. To properly mount a response, T cells use extracellular receptors to sense their environment and transduce signals to intracellular signaling networks. Following ligation of the T cell receptor (TCR) to an antigen, both phospholipid and kinase signaling networks are activated. Our working hypothesis is that T cells encode different signaling inputs by generating qualitatively different phosphoproteomes that drive alternate cellular differentiation programs. We are also interested in defining how phospholipid second messengers control T cell signaling. We utilize a combination of cellular immunology, mass spectrometry, biophysics, high resolution microscopy, high content imaging, chemical genetics and single cell assays to study the mechanisms underlying T cell activation. We utilize the mechanistic insight gained from signaling studies to rationally alter pathways to control T cell activation and differentiation in the context of multiple infection and autoimmune models. Current projects in the lab include: 1) identifying Molecular mechanisms that encode TCR signal strength, 2) defining mechanisms of cross-talk between TCR and cytokine signaling networks and 3) determining the proteomic differences that define memory T cell recall responses.