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Brigitta Stockinger

Researcher at Francis Crick Institute

Publications -  143
Citations -  25195

Brigitta Stockinger is an academic researcher from Francis Crick Institute. The author has contributed to research in topics: T cell & Cytotoxic T cell. The author has an hindex of 62, co-authored 137 publications receiving 22395 citations. Previous affiliations of Brigitta Stockinger include Medical Research Council & Max Planck Society.

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TGFβ in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-Producing T cells

TL;DR: The data indicate that, in the presence of IL-6, TGFbeta1 subverts Th1 and Th2 differentiation for the generation ofIL-17-producing T cells.
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The aryl hydrocarbon receptor links TH17-cell-mediated autoimmunity to environmental toxins.

TL;DR: It is shown that in the CD4+ T-cell lineage of mice AHR expression is restricted to the TH17 cell subset and its ligation results in the production of the TH16 cytokine interleukin (IL)-22, and AHR ligands may represent co-factors in the development of autoimmune diseases.
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Transforming growth factor-beta 'reprograms' the differentiation of T helper 2 cells and promotes an interleukin 9-producing subset

TL;DR: It is shown that transforming growth factor-β constitutes a regulatory 'switch' that in combination with other cytokines can 'reprogram' effector T cell differentiation along different pathways.
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Fate mapping of IL-17-producing T cells in inflammatory responses

TL;DR: A reporter mouse strain designed to map the fate of cells that have activated interleukin 17A (IL-17A) allows the actual functional fate of effector T cells to be related to TH17 developmental origin regardless of IL-17 expression.
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Interleukin-17-Producing γδ T Cells Selectively Expand in Response to Pathogen Products and Environmental Signals

TL;DR: In innate receptor expression linked with IL-17 production characterizes TCRgammadelta T cells as an efficient first line of defense that can orchestrate an inflammatory response to pathogen-derived as well as environmental signals long before Th17 cells have sensed bacterial invasion.