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Joris van der Veeken

Researcher at Memorial Sloan Kettering Cancer Center

Publications -  21
Citations -  4425

Joris van der Veeken is an academic researcher from Memorial Sloan Kettering Cancer Center. The author has contributed to research in topics: FOXP3 & Transcription factor. The author has an hindex of 12, co-authored 18 publications receiving 3292 citations. Previous affiliations of Joris van der Veeken include Cornell University & Research Institute of Molecular Pathology.

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Metabolites produced by commensal bacteria promote peripheral regulatory T-cell generation

TL;DR: The results suggest that bacterial metabolites mediate communication between the commensal microbiota and the immune system, affecting the balance between pro- and anti-inflammatory mechanisms.
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Control of the Inheritance of Regulatory T Cell Identity by a cis Element in the Foxp3 Locus

TL;DR: CNS2-mediated stable inheritance of Foxp3 expression is critical for adequate suppression of diverse types of chronic inflammation by Treg cells and prevents their differentiation into inflammatory effector cells.
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Inflammation-induced repression of chromatin bound by the transcription factor Foxp3 in regulatory T cells

TL;DR: Foxp3 poises its targets for repression by facilitating the formation of repressive chromatin in Treg cells upon their activation in response to inflammatory cues.
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Downregulation of EGFR by a novel multivalent nanobody-liposome platform

TL;DR: In this study, a multivalent platform is presented, consisting of nanobodies recognizing the ectodomain of EGFR (EGa1) coupled to PEG-liposomes, and the in vitro and in vivo effects of this system on EGFR internalization and downregulation were investigated.
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Memory of Inflammation in Regulatory T Cells.

TL;DR: It is found that the inflammation-experienced Treg cell population reversed many activation-induced changes and lost its enhanced suppressive function over time, suggesting the "memory-less" potentiation of Treg suppressor function may help avoid a state of generalized immunosuppression that could otherwise result from repeated activation.