Dr. Andrea J. Tenner is a leader in the complement research field, and has been applying her expertise to study how this system influences protective response to pathogens and injury, modulates immune responses, contributes to neuroprotection and when dysregulated causes detrimental inflammatory disorders particularly in neurodegenerative diseases such as Alzheimer’s disease. Dr. Tenner has functionally characterized immune modulatory functions of complement proteins C1q independent of other components of the complement system demonstrating that while C1q plays a role in the efficiency of phagocytosis of apoptotic cells and cellular debris, it importantly induces the expression of anti inflammatory signals by human macrophages and dendritic cells that suppress proliferation of inflammatory, but not regulatory, T cell subsets. C1q induced similar anti-inflammatory polarization of microglia, the macrophages of the brain. Her laboratory has also explored the consequences of activation of the entire complement pathway by fibrillar (ß-sheet) amyloid plaques in Alzheimer’s disease, demonstrating that the complement activation product C5a can contribute to inflammation and progression of Alzheimer’s disease in mouse models. The potential targeting of this C5a-C5aR1 axis to slow or stop progression of this and other neurodegenerative diseases is a major focus of her lab today. Models of AD pathology combined with characterization and use of a conditional knock out of the specific complement component, C1q, are being used to distinguish pathways early in the progression of the disease vs late in the disease (as would occur at the time of clinical presentation in human AD). The expression and function of human CR1 in brain and peripheral blood from individuals diagnosed with AD or MCI compared with non-demented human is also investigated. Another current interest is on neuroprotection and potential therapeutic targets to enhance neuron survival and function. The overall goal is to understand the molecular interactions involved such that therapeutic interventions to limit damaging inflammation or enhance appropriate immune responses can be designed.
Dr. Tenner earned her Ph.D. at the University of California, San Diego, and subsequently conducted research at Scripps Institute and Research Foundation, La Jolla, California, the NIH, and the American Red Cross Holland Laboratories in Rockville, Maryland. In 1992, Dr. Tenner joined University of California, Irvine, where she is currently Professor of Molecular Biology and Biochemistry, Pathology and Laboratory Medicine, and Neurobiology and Behavior. Dr. Tenner served as Associate Dean for Research, UCI School of Biological Sciences (2007-2012), and Director of the UC, Irvine Institute for Memory Impairment and Neurological Disorders (UC iMIND) (2014-2016). Dr. Tenner’s professional activities have included Section Editor for the Journal of Immunology, member of the NIH study sections and other grant reviewing committees, Councilor for the Society of Leukocyte Biology (and was awarded an Honorary Life Member of the Society), and President of the International Complement Society. Dr. Tenner received the UCI Emeritae/I Association Faculty Mentorship Award, and was the recipient of the UC, Irvine Daniel G. Aldrich, Jr. Distinguished University Service Award, an award conferred to those achieving distinction in their scholarly pursuits and have also made sustained and outstanding contributions through service to the University.