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Thomas Brunner

Researcher at University of Konstanz

Publications -  511
Citations -  26076

Thomas Brunner is an academic researcher from University of Konstanz. The author has contributed to research in topics: Apoptosis & Medicine. The author has an hindex of 75, co-authored 448 publications receiving 23438 citations. Previous affiliations of Thomas Brunner include University Medical Center Freiburg & University of Oxford.

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Fas Ligand-Induced Apoptosis as a Mechanism of Immune Privilege

TL;DR: Inflammatory cells entering the anterior chamber of the eye in response to viral infection underwent apoptosis that was dependent on Fas (CD95)-Fas ligand (FasL) and produced no tissue damage.
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Cell-autonomous Fas (CD95)/Fas-ligand interaction mediates activation-induced apoptosis in T-cell hybridomas

TL;DR: This work shows that the Fas/CD95 receptor, which can transduce a potent apoptotic signal when ligated, is rapidly expressed following activation of T-cell hybridomas, as is its functional, membrane-bound ligand8.
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Calpain-mediated cleavage of Atg5 switches autophagy to apoptosis.

TL;DR: Calpain-mediated Atg5 cleavage provokes apoptotic cell death, therefore, represents a molecular link between autophagy and apoptosis — a finding with potential importance for clinical anticancer therapies.
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DNA Damaging Agents Induce Expression of Fas Ligand and Subsequent Apoptosis in T Lymphocytes via the Activation of NF-κB and AP-1

TL;DR: It is reported that activation of the two transcription factors NF-kappa B and AP-1 is crucially involved in FasL expression induced by etoposid, teniposide, and UV irradiation and contributes to stress-induced apoptosis via the expression of FasL.
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Induction of human IgE synthesis in B cells by mast cells and basophils

TL;DR: It is reported that, in the presence of IL-4, mast and basophilic cell lines can provide the cell contact signals that are required for IgE synthesis, suggesting that mast cells and Basophils may play a key role in allergy not only by producing inflammatory mediators, but also by directly regulating IgE production independently of T cells.