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Welcome to the Sansing Lab

brain with colored sections
The Sansing lab studies the responses of the immune system after acute brain injuries, including stroke and intracerebral hemorrhage, a devastating type of stroke that occurs when a blood vessel within the brain ruptures. Once injury occurs, microglia, the resident immune cells of the brain, become activated, and there is recruitment of blood leukocytes, including neutrophils, monocytes, and T cells, into the brain. Our work aims to untangle the kinetics and activation states of these immune cells and discover which responses are injurious and should be inhibited, and which responses contribute to recovery and should be augmented. The overall goal of our research is to discover fundamental mechanisms of neuroinflammation and identify new, therapeutic targets that modulate immune responses to maximize recovery.

About

Hemorrhage in the brain and different immune responses
The Sansing lab has focused on inflammatory mechanisms of secondary brain injury and recovery after stroke. Using the genetic tractability of experimental models, we have determined fundamental roles for monocyte/macrophages in initial injury, determined that efferocytosis of apoptotic debris leads to phenotype modulation in the cells and drives their contribution to recovery, and determined that microglia depend on TGFβ signaling to promote repair. We have worked extensively in human immunology by transcriptionally profiling leukocytes from the brains of patients by RNA-seq and single cell RNA-seq as examining mechanisms of leukocyte responses in human cellular assays. We apply these methods to patient samples from cohort studies and clinical trials as well as pathology specimens to further our work in the translational realm.