Overview

I am an assistant professor in the Department of Neurosurgery at Duke University. I am interested in mechanisms of immunosuppression following various neurological insults. I am a classically trained Immunologists. My PhD work was focused on drug-induced immunosuppression and mechanisms of immune reconstitution in mouse models of transplantation. Briefly, I discovered that a common lymphocyte depleting drug, ATG, leaves behind a population of memory CD4 T cells. These residual memory CD4 T cells are required for reconstitution of CD8 T cells and optimal thymic function to produce new T cells. 

As a postdoc, I was fascinated by the neuroimmune connections in brain cancer and during other brain injuries. My expertise in mechanisms of immunosuppression and immune reconstitution allowed me to study neurological-injury induced immunosuppression. Both acute and chronic neurological diseases induce severe peripheral immunosuppression including low CD4 T cell count, immune organ atrophy, and lower MHCII expression on APCs. For example, GBM patients have CD4 T cell counts as low as AIDS patients. Yet, the mechanisms of such profound immunosuppression remains unknown. During my postdoc, I was able to determine hallmark features of peripheral immunosuppression described in patients also occur in mice using novel mouse models. We determined that soluble actors released during brain injury mediate most hallmark features of immunosuppression using parabiosis. These included low CD4 T cells count, MHCII downregulation, and thymic involution. We further discovered that serum-derived non-steroidal factors with molecular weights larger than 100kDa are responsible for the peripheral immunosuppression in mouse models of GBM. Similar soluble factor mediated immunosuppression was in play in other non-cancerous brain injuries as well.   
I am continuing this line of work and investigating the identity of soluble factors involved in mediating peripheral immunosuppression in GBM and other brain injuries in my independent laboratory. GBM is incurable and associated with severe immunosuppression systemically. Most immune-modulating therapies will fail in the presence of severe immunosuppression. Our goal is to determine what causes peripheral immunosuppression and devise strategies to reverse it. This is the first step in developing novel therapeutics for GBM patients. Our work is also relevant to other neurological diseases and will be applicable to a large cohort of patients with acute and chronic neurological diseases. 

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