Ruth Napier, Ph.D., receives Bruckel Early Career Investigator Award

Left to right: Ruth J. Napier, Holly Rosenzweig, Ellen Lee, Emily Vance, Sydney Lashley, Kofi Asare-Konadu, Nikita Farhaj, and Kylie Koney.

Ruth J. Napier, Ph.D., has been named recipient of the 2021 Spondylitis Association of America/Bruckel Early Career Investigator Award. The award is given annually to the early career investigator who shows the most promise to contribute to the understanding or therapy of axial spondyloarthritis, an inflammatory arthritis primarily affects the spine and the sacroiliac joints that connect the lower spine to the pelvis.

Understanding the intersections of microbes and autoimmunity to learn more about the pathogenesis of inflammatory diseases — and contribute novel drug targets for future therapies.

The Napier lab studies the cellular and molecular mechanisms by which CD4+ T helper (Th) cells — which are integral to the adaptive immune system and the body’s ability to fight infection — become dysregulated and cause sterile inflammation. Napier, principal investigator of this translational immunology laboratory at the VA Portland Health Care System, is also an assistant professor of molecular microbiology and immunology in the OHSU School of Medicine.

Ruth Napier, Ph.D., VA Portland Health Care System and OHSU Department of Molecular Microbiology and Immunology
Ruth J. Napier, Ph.D., recipient of the 2021 SAA Bruckel Early Career Investigator Award

Napier pairs basic research studies in experimental mouse models of arthritis and uveitis with clinical studies done with blood samples from patients with rheumatoid arthritis, ankylosing spondylitis and Blau Syndrome.

In her ankylosing spondylitis (AS) research, Napier is investigating how microbial-signaling molecules like CARD9 control the disease. She recently showed that microbial exposure causes CARD9 to promote a pathogenic neutrophil response, which in turn activates pathogenic CD4+ T cells to produce IL-17 and cause AS. These data are immediately clinically relevant and information gained in these studies will be used to help design future therapeutics to treat AS.

Napier’s October 2020 manuscript on the protein coding gene NOD2, published in Nature Communications, also has clinical implications. The research demonstrates that NOD2 is controlling T cells directly by suppressing markers associated with autoreactivity. This research, which clarified the way NOD2 is functioning in the T cell, opened up opportunities for T cell-based therapies that are well-tolerated and already readily available.