SCRC

Bolhson, Suzanne, Ph.D.

Section 1

Suzanne Bohlson, Ph.D.

Professor

Biography

Dr. Bohlson obtained her B.S. in Biology from University of California- Irvine, her M.S. in Biomedical Science/Immunology from Washington University in St. Louis and her Ph.D. in Biology from the University of Notre Dame. After a postdoctoral fellowship at University of California- Irvine, she began her first faculty position at Indiana University School of Medicine- South Bend campus in 2006 where she stayed util 2013. From 2013- 2019 she was on faculty of Des Moines University and then moved to UC Irvine in 2019 as a Professor of Teaching and Director of the Master of Science in Biotechnology program in the Department of Molecular Biology and Biochemistry..

Research in Lay Terms

My laboratory and research efforts have focused on the innate immune system.  As the first line of defense, the innate immune system must distinguish infectious microbes or dangerous self-molecules from innocuous materials (e.g. apoptotic cells).  The interactions governing this recognition phase, and the signals that ensue, contribute to the subsequent adaptive immune response and outcome of infection and/or tissue distress.  C1q is a soluble protein found in the blood that regulates this recognition phase, and deficiency in C1q results autoimmunity.  We are exploring the different mechanisms by which C1q enhances cell function and regulates inflammation, thought to be important in the prevention of autoimmunity. C1q is also important in regulating inflammation in the brain, and in collaboration with the Tenner lab at UCI, we are exploring the influence of C1q on neuroinflammation using animal models as well as human iPSC-derived neurons and microglia in the context of Alzheimer’s disease (AD)- associated pathology. C1q protects neurons from injury associated with AD and we are investigating the molecular mechanism of neuroprotection, as well as its translational potential, with the eventual goal of developing therapeutics to promote neuronal resilience in AD.