Andrew L. Snow, Ph.D., Assistant Professor
B.S., Biology, Duke University
Ph.D., Immunology, Stanford University
Postdoctoral Training, National Institutes of Health
4301 Jones Bridge Road, C2013
Bethesda, MD 20814
Phone: 301-295-3267
Email: asnow@usuhs.mil
Antigen Receptor Signaling & Lymphocyte Homeostasis
The overall number and associated functions of white blood cells known as T and B lymphocytes are carefully regulated by biochemical signals that can activate or kill a given cell during different phases of an immune response. Many of these signals are initiated by engagement of the antigen receptor on the cell surface. For example, repeated engagement of the T cell receptor (TCR) on an activated T cell triggers a self-regulatory apoptosis program known as restimulation-induced cell death (RICD). However, the intracellular biochemical processes that determine the ultimate outcome of antigen receptor signaling in a "naïve" versus a "previously activated" lymphocyte, including survival, proliferation, or programmed cell death, remain poorly defined. The major focus of our laboratory is to identify and characterize those genes, proteins, and their associated modifications that distinguish between survival and death signaled through antigen receptor stimulation in both T and B cells. We are also interested in elucidating how the loss or mutation of key genes (e.g. SLAM-associated protein (SAP)) alters apoptosis sensitivity and contributes to dysregulation of immune homeostasis. Our goal in studying these molecular pathways is to advance our knowledge of how the immune system maintains balanced responses, and illuminate new genes and biomarkers that explain aberrant lymphocyte regulation in diseases involving excessive lymphocyte proliferation and/or leukemia and lymphoma.
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Uniformed Services University of the Health Sciences
Department of Pharmacology
4301 Jones Bridge Road
Bethesda, MD 20814
Tel 301-295-3223
FAX 301-295-3220