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Jeroen Raes

Researcher at Katholieke Universiteit Leuven

Publications -  293
Citations -  85097

Jeroen Raes is an academic researcher from Katholieke Universiteit Leuven. The author has contributed to research in topics: Microbiome & Medicine. The author has an hindex of 84, co-authored 240 publications receiving 66805 citations. Previous affiliations of Jeroen Raes include Flanders Institute for Biotechnology & Université catholique de Louvain.

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Microbiota, not host origin drives ex vivo intestinal epithelial responses

TL;DR: It is concluded that not the epithelial cell origin (UC versus non-IBD) but the microbial donor drives transcriptomic responses, as exposure to UC microbiota was sufficient to induce stress responses in all epithelial cells.
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Comparisons of gut microbiota profiles in wild-type and gelatinase B/matrix metalloproteinase-9-deficient mice in acute DSS-induced colitis.

TL;DR: Changes in fecal microbiota composition were not significantly altered in MMP-9-deficient mice compared to wild-type littermates, but instead were mainly driven by DSS-induced colonic inflammation.
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Unstable regulatory T cells, enriched for naïve and Nrp1neg cells, are purged after fate challenge.

TL;DR: In this paper, the authors used a murine genetic fate-mapping system to show that Treg stability is maintained even during exposure to a complex microbial/antigenic environment, and demonstrate that the observed plasticity of Tregs after adoptive transfer into a lymphopenic environment is a property limited to only a subset of the Treg population.
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High Serum Vitamin D Concentrations, Induced via Diet, Trigger Immune and Intestinal Microbiota Alterations Leading to Type 1 Diabetes Protection in NOD Mice

TL;DR: Dietary vitamin D reduced T1D incidence in female NOD mice at a dose of 800, but not of 400, IU/day, and was accompanied by an expansion of Treg cells in various lymphoid organs and an altered intestinal microbiota signature, which significantly influenced the inter-individual microbiota variation at the genus level.