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Katharine A. Whartenby

Researcher at Johns Hopkins University School of Medicine

Publications -  47
Citations -  3191

Katharine A. Whartenby is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: T cell & Experimental autoimmune encephalomyelitis. The author has an hindex of 22, co-authored 46 publications receiving 2867 citations. Previous affiliations of Katharine A. Whartenby include Johns Hopkins University & University of Rochester Medical Center.

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The "bystander effect": tumor regression when a fraction of the tumor mass is genetically modified.

TL;DR: It is demonstrated that genetic modification of tumor cells may be useful for developing cancer therapies and the mechanism of this "bystander effect" was related to the process of apoptotic cell death when HSV-TK-positive cells were exposed to GCV.
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Mesenchymal stem cells: Emerging mechanisms of immunomodulation and therapy

TL;DR: The full range of MSC-mediated immune-modulation remains incompletely understood, as emerging reports also reveal that MSCs can adopt an immunogenic phenotype, stimulate immune cells, and yield seemingly contradictory results in experimental animal models of inflammatory disease.
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Role of PD-1 and its ligand, B7-H1, in early fate decisions of CD8 T cells

TL;DR: B7-H1:PD-1 interactions regulate early T-cell-fate decisions and it is demonstrated that CD8 T cells specific for influenza hemagglutinin expressed as a self-antigen become functionally tolerized and express high levels of surface PD-1 by the time of their first cell division.
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Human iPSC-derived blood-brain barrier microvessels: validation of barrier function and endothelial cell behavior.

TL;DR: Human iPSC-derived blood-brain barrier microvessels support quantitative analysis of barrier function and endothelial cell dynamics in quiescence and in response to biologically- and clinically-relevant perturbations.
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Inhibition of FLT3 signaling targets DCs to ameliorate autoimmune disease.

TL;DR: Results of the studies show that inhibition of FLT3 signaling induces apoptosis in both mouse and human DCs, and thus is a potential target for immune suppression, suggesting a potential avenue for treating autoimmune disease.