We are an interdisciplinary, collaborative team with expertise in immunology, neuroinflammation, and autoimmunity. We strive to understand the fundamental molecular, cellular, and genetic mechanisms that drive debilitating neurodegenerative and neuropsychiatric diseases. One of our primary goals is to translate these discoveries into therapeutic strategies targeting these disease mechanisms. Areas of research include:
Neuropsychiatric Systemic Lupus Erythematosus (NPSLE):
Neuropsychiatric symptoms are among the most challenging manifestations experienced by a significant subset of lupus patients and are a major contributor to morbidity and mortality associated with lupus autoimmunity. Little is understood about why certain patients develop central nervous system (CNS) involvement. The Hsieh Lab investigates genetic variants in lupus and NPSLE patients to better understand the links between autoimmunity and neuroinflammation. We collaborate with partners at UCSF to study the CLUES clinical repository of longitudinal lupus samples. Complementing these human studies, we also use a preclinical mouse model of NPSLE-like disease to dissect the molecular and cellular mechanisms underlying autoimmunity and CNS pathology.
Frontotemporal Dementia (FTD):
FTD is a neurodegenerative disorder caused by progressive degeneration of the frontal and temporal lobes of the brain, regions critical for decision-making, behavioral control, emotion, and language. In individuals under the age of 60, FTD is the most common cause of dementia. It is a fatal disease with no currently approved disease-modifying therapies. FTD also shares significant genetic overlap with Amyotrophic Lateral Sclerosis (ALS). Our lab seeks to understand the genetic and immune-mediated cellular mechanisms that contribute to the onset and progression of FTD.
Traumatic Brain Injury (TBI):
TBI can lead to long-term cognitive and motor impairments and remains a major public health issue, with approximately 3 million TBI-related emergency department visits, hospitalizations, and deaths occurring annually in the United States. Given the urgent need for therapies that improve outcomes after TBI, our lab uses preclinical mouse models, genetic approaches, and pharmacological interventions to identify targets that may reduce the behavioral deficits associated with brain injury. Our work has identified important roles for inflammatory brain-infiltrating monocytes and type I interferon–driven microglia in the pathogenesis of TBI.
Please reach out if you are interested in joining the lab or pursuing scientific collaborations.
Also visit our San Francisco VA Immunology website.