OREGON HEALTH & SCIENCE UNIVERSITY, PROFESSOR

Dr. Louis J. Picker is the Associate Director of the Vaccine and Gene Therapy Institute, a Senior Scientist in the Pathobiology and Immunology Division of the Oregon National Primate Research Center, and a Professor of Pathology at the Oregon Health & Science University.

Dr. Picker was recruited to OHSU in 2000 from the Department of Pathology at the University of Texas Southwestern Medical Center at Dallas where he served as a Principal Investigator, Medical Director of the Flow Cytometry and Clinical Immunology Laboratory, and Co-Director of the Division of Hematopathology and Immunology.

He received his medical degree at the University of California, San Francisco in 1982, did an internship, residency, and chief residency in Anatomic and Clinical Pathology at the Beth Israel Hospital and Harvard Medical School in Boston, Massachusetts from 1982-86, and received advanced training in Immunopathology and Experimental Pathology at Stanford University Medical Center in Palo Alto, California from 1986-89.

Dr. Picker is known for his work elucidating human/nonhuman primate (NHP) memory T cell biology (including mechanisms of memory T cell homing, functional differentiation and homeostasis, mechanisms of protection against persistent pathogens, and the immunopathogenesis of AIDS), and the preclinical development HIV/AIDS vaccine and cure concepts using NHP models.

The central role of FcRn in regulating immunoglobulin G (IgG) persistence and transport provides opportunities for targeting this receptor in multiple different diagnostic and therapeutic situations. The engineering of IgGs with higher affinity for FcRn can be used to produce antibodies with longer in vivo half-lives, but only if the low affinity of the IgG-FcRninteraction at near neutral pH is retained. Conversely, an engineered IgG or Fc fragmentwith increased affinity for FcRn at both acidic and near neutral pH acts as a potent inhibitor of FcRn. Consequently, such an antibody (‘Abdeg’, for antibody that enhancesIgG degradation) can lower the levels of endogenous IgG and has led to the FcRn antagonist, efgartigimod, that has been developed by argenx and recently approved for the treatment of myasthenia gravis. Our recent work has also resulted in the generation of engineered Fc-fusions that selectively clear antigen-specific antibodies (‘Seldegs’, for selective degradation). Developments related to the modulation of the dynamic behavior of IgG in the bodywill be presented.