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Derek Sant'Angelo
Associate
Professor
Division Chief, Developmental Biology
RWJMS -
Dept. of Pediatrics
The Child Health Institute of NJ
89 French Street, Room 4220
New Brunswick. NJ 08903
(732) 235-9394
FAX - 9333
santandb@umdnj.edu |
Innate T cells; transcription factors; autoimmunity;
lineage commitment; immune system development; immunotherapy
Transcriptional control of innate T cell effector functions.
A functional immune system is dependent upon a wide variety of
lymphocytes, such as T cells and B cells, and myelocytes, such as
macrophages and dendritic cells. Specialization of function of these
various cell types is fundamental for both successful immune responses
against pathogens and for immunosurveillance against cancer. Our lab is
interested in 1) understanding the factors that control lymphocyte
development and 2) determining if these factors can used to modify or
enhance T cell responses against cancer.
Innate T cells, such as natural killer T cells (NKT cells), are extremely
potent "first responders" to infection. The aggressive nature of innate T
cells has also made them attractive targets for immunotherapy - several
clinical trials are in progress. Our lab has recently identified a BTB-ZF
transcriptional repressor that controls the development of the innate T
cells. In the absence of this factor, innate T cells default to the
conventional CD4 T cell lineage.
Alternatively, conventional T cells are redirected into the innate T cell
lineage by ectopic expression of the transcription factor.
We are working to discover what genes are being repressed by this BTB-ZF
transcription factor; how the factor mediates suppression; signaling
events that lead to the factor being expressed specifically in innate T
cells and control of the expression of the transcription factor.
Furthermore, we are determining if redirected expression of the BTB-ZF
gene will enhance the activity of conventional T cells.
Finally, we are interested in learning if spontaneous expression of the
factor in conventional T cells can lead to autoimmunity.
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