Andrew L. Snow, Ph.D.

Andrew L. Snow, Ph.D.

andrew snow

Name: Andrew L. Snow, Ph.D.

Department of Primary Appointment: Pharmacology
Position: USU Faculty
Title: Assistant Professor

Affiliated Departments: Molecular & Cell Biology, Emerging Infectious Diseases

Research Interests:
Antigen Receptor Signaling & Lymphocyte Homeostasis

Email: andrew.snow@usuhs.edu (link sends e-mail)
Office Phone: (301) 295-3267
Fax Number: (301) 295-3220
Room: C2013

Links
Department Website
PubMed Listing

Profile

Profile

  • B.S., Biology, Duke University
  • Ph.D., Immunology, Stanford University
  • Postdoctoral Training, National Institutes of Health

Antigen Receptor Signaling & Lymphocyte Homeostasis

Antigen Receptor Signaling and 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 "na?ve" 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.