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Svenja Debey

Researcher at University of Cologne

Publications -  13
Citations -  1925

Svenja Debey is an academic researcher from University of Cologne. The author has contributed to research in topics: Cytotoxic T cell & T cell. The author has an hindex of 10, co-authored 13 publications receiving 1848 citations. Previous affiliations of Svenja Debey include University of Pennsylvania & University of Bonn.

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Salicylic Acid–Independent ENHANCED DISEASE SUSCEPTIBILITY1 Signaling in Arabidopsis Immunity and Cell Death Is Regulated by the Monooxygenase FMO1 and the Nudix Hydrolase NUDT7

TL;DR: Two new immune regulators are defined through analysis of corresponding Arabidopsis loss-of-function insertion mutants, and it is found that SA antagonizes initiation of cell death and stunting of growth in nudt7 mutants.
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CD25 and indoleamine 2,3-dioxygenase are up-regulated by prostaglandin E2 and expressed by tumor-associated dendritic cells in vivo: additional mechanisms of T-cell inhibition.

TL;DR: PGE2 is suggested to be a mediator of early events during induction of immune tolerance in cancer by demonstrating a concomitant induction of IDO and secretion of soluble CD25 after DC maturation in the presence of PGE2.
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Comparison of different isolation techniques prior gene expression profiling of blood derived cells: impact on physiological responses, on overall expression and the role of different cell types.

TL;DR: It is concluded that for large clinical studies, it is crucial to reduce maximally the time to RNA isolation to optimize clinical studies applying gene expression analysis of peripheral blood to exploit drug responses and to better understand changes associated with disease.
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Indoleamine 2,3-dioxygenase–expressing dendritic cells form suppurative granulomas following Listeria monocytogenes infection

TL;DR: It is shown in human listeriosis that DCs expressing indoleamine 2,3-dioxygenase (IDO), together with macrophages, are major cellular components of suppurative granulomas in vivo and in vitro that IDO induction is TNF-alpha dependent.