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Carl Weidinger

Researcher at Humboldt University of Berlin

Publications -  12
Citations -  429

Carl Weidinger is an academic researcher from Humboldt University of Berlin. The author has contributed to research in topics: Immune system & Inflammation. The author has an hindex of 10, co-authored 12 publications receiving 241 citations. Previous affiliations of Carl Weidinger include Charité.

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Functional Role of Transient Receptor Potential Channels in Immune Cells and Epithelia.

TL;DR: An overview about TRP-mediated effects in immune and epithelial cells with an emphasis on mucosal immunology of the gut is provided and understanding of its molecular mechanisms paves the way to novel clinical approaches for the treatment of various inflammatory disorders including IBD.
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Adipokines and Their Role in Intestinal Inflammation

TL;DR: The present review selected the four adipokines adiponectin, apelin, chemerin, and leptin and provides a working model based on the available literature how these factors participate in the maintenance of intestinal immune homeostasis.
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Anti-Adhesion Therapies in Inflammatory Bowel Disease—Molecular and Clinical Aspects

TL;DR: The fundamental basis of intestinal T cell homing is summarized, the molecular groundwork underlying current and potential future anti-adhesion therapies are explained and the outlook to the future of anti-integrin antibodies and inhibitors is given.
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Human small intestinal infection by SARS-CoV-2 is characterized by a mucosal infiltration with activated CD8 + T cells.

TL;DR: In this article, the authors used qRT-PCR and immunohistochemistry to detect SARS-CoV-2 RNA and nucleocapsid protein in duodenal mucosa and identified histomorphological changes of the epithelium, which were characterized by an accumulation of activated intraepithelial CD8+ T cells as well as epithelial apoptosis and subsequent regenerative proliferation.
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HDAC inhibitors promote intestinal epithelial regeneration via autocrine TGFβ1 signalling in inflammation

TL;DR: In human and murine colonic epithelial cell lines, the presence of the HDAC inhibitors Givinostat and VorInostat not only improved transepithelial electrical resistance under inflammatory conditions but also attenuated the passage of macromolecules across the epithelial monolayer.