Graduate Studies Faculty

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Jeffrey C. Nolz, Ph.D.

Assistant Professor
Admin Unit: SOM-Molecular Microbiology & Immunology Department
Phone: 503-494-1356
Office: RJH 6516
Mail Code: L220
Cell & Developmental Biology
Molecular Microbiology & Immunology
Program in Molecular & Cellular Biosciences
Research Interests:
» PubMed Listing
Preceptor Rotations
Academic Term Available Summer 2017 Yes Fall 2017 Yes Winter 2017 Yes Spring 2017 Yes
Faculty Mentorship
Dr. Nolz is available as a mentor for 2016-2017. Dr. Nolz is available as a mentor for 2017-2018.
Trafficking of T cells out of the circulation and into various tissues is a highly orchestrated process involving multiple receptor – ligand interactions.  In my laboratory, we utilize a wide variety of disease models combined with molecular and cellular approaches aimed at ultimately understanding the biochemical signals that dictate T cell localization in vivo.  The selectin family of proteins (L-, P-, and E-selectin) play a critical role in regulating immune cell trafficking and facilitate the initial interactions between T cells and vascular endothelium prior to chemokine-mediated signaling and integrin activation.  Importantly, ligands for selectins require post-translational glycosylation to become functional and both CD8+ and CD4+ T cells exhibit dynamic regulation of the enzymes that are responsible for generating these O-linked glycan structures.  Furthermore, we have recently discovered that the generation of core 2 O-glycans within memory CD8+ T cell populations occurs in an antigen-independent manner, but rather is controlled by inflammatory cytokines.   In addition, we have shown that this is a major regulatory mechanism controlling memory CD8+ T cell recruitment to inflamed tissue prior to antigen re-encounter.  Thus, a comprehensive understanding of the molecular and biological mechanisms that regulate T cell O-glycan synthesis and trafficking could ultimately result in new disease prevention strategies by therapeutically directing (for vaccines and tumor immunotherapy) or inhibiting (for autoimmunity) T cell recruitment to target tissues.