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Novel Calcium Dependent Mechanisms of NF-kappaB Activation Regulate Lymphocyte Tolerance & Immunity
Start Date: 5/31/2018Start Time: 2:00 PM
End Date: 5/31/2018End Time: 4:00 PM

Event Description
BIOMED PhD Thesis Defense

Title:
Novel Calcium Dependent Mechanisms of NF-kappaB Activation Regulate Lymphocyte Tolerance and Immunity

Speaker:
Corbett T. Berry, MD/PhD Candidate, School of Biomedical Engineering, Science and Health Systems

Advisors:
Bruce D. Freedman, VMD, PhD, Associate Professor, School of Veterinary Medicine, University of Pennsylvania

Uri Hershberg, PhD, Associate Professor, School of Biomedical Engineering, Science and Health Systems, Drexel University

Abstract:
Antigen induced Ca2+ signals regulate the development of immunity and tolerance. These signals are generated when antigen binds cognate receptors on lymphocytes and triggers Ca2+ entry into the cytoplasm. Indeed, patients with functional defects in the ER transmembrane Ca2+-sensing STIM proteins, or the STIM-activated Ca2+ entry channel Orai, exhibit devastating immunodeficiency and autoimmunity.

This immune phenotype occurs as a result of dysfunctional lymphocyte development and function principally through aberrant activation of Ca2+ dependent transcription factors including NFAT and NF-kB. While the role of Ca2+ signaling in NFAT activation and signaling is well established, a wide appreciation and mechanistic understanding of how Ca2+ signals also shape the activation and specificity of NF-kB dependent gene expression is incomplete.

In these studies, we establish that STIM/Orai dependent Ca2+ entry regulates multiple checkpoints in NF-kB signaling, but also NF-kB independent pathways to regulate lymphocyte survival, proliferation, and differentiation.
Contact Information:
Name: Ken Barbee
Phone: 215-895-1335
Email: barbee@drexel.edu
Corbett Berry
Location:
Curtis Hall, Room 341, located at 32nd and Chestnut Streets
Audience:
  • Undergraduate Students
  • Graduate Students
  • Faculty
  • Staff

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