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John Huizar, MD

2024 Recipient of the Gary S. Gilkeson Career Development Award

University of California, Berkeley 

Mentor(s): Gregory Barton, PhD 

Project Title: Decoding innate immune dysregulation in human autoimmune disease 

About the Researcher 

John P. Huizar, MD, completed his undergraduate medical education at UCSF, where he undertook a two-year research fellowship in the lab of Dr. Julie Zikherman studying the control of B cell activation. He went on to complete his internal medicine residency and clinical fellowship in adult Rheumatology at UCSF. He is now an Adjunct Professor of Rheumatology at UCSF with a practice focus at Zuckerberg San Francisco General Hospital, the nucleus of San Francisco’s safety net health system. 

Dr. Huizar is presently in the midst of a post-doctoral research fellowship in the lab of Dr. Gregory Barton, PhD, where he is working to understand how the body’s innate or “first-line” immune responses to self and foreign RNA and DNA become dysregulated in lupus. The only lupus therapy that currently targets this process directly is hydroxychloroquine (and it’s cousins), and Dr. Huizar hopes that insights from this work will not only expand the pipeline of safe and effective lupus therapies, but also help elucidate why lupus manifests so differently in different individuals. 

Project Summary 

We want to understand how a person's genetic makeup influences their risk of lupus. In lupus and related autoimmune diseases, the innate immune system (the body’s first line of defense) loses the ability to distinguish self DNA and RNA from foreign, pathogen-derived DNA and RNA. Dr. Huizar and his colleagues have used new approaches including CRISPR technology to expand the list of culprit genes that may be responsible for innate immune system dysfunction in SLE. His work with the LFA will marry genome sequence information from people living with lupus to this new information about candidate lupus driver genes, and may ultimately expand our understanding of how individual genetic makeup contributes to both the risk of developing lupus, and the distinct profile of lupus symptoms experienced by each affected person. We hope that this information will ultimately improve the design of lupus clinical trials and enable personalized therapy decisions for people living with lupus and other autoimmune diseases.