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Steven J. Van Dyken

Researcher at Washington University in St. Louis

Publications -  43
Citations -  4149

Steven J. Van Dyken is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Immune system & Innate lymphoid cell. The author has an hindex of 19, co-authored 33 publications receiving 3308 citations. Previous affiliations of Steven J. Van Dyken include University of California, San Francisco & University of California, San Diego.

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Type 2 innate lymphoid cells control eosinophil homeostasis

TL;DR: It is shown that serum IL-5 levels are maintained by long-lived type 2 innate lymphoid cells (ILC2) resident in peripheral tissues, and this dissociated regulation can be tuned by nutrient intake and central circadian rhythms.
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Innate lymphoid type 2 cells sustain visceral adipose tissue eosinophils and alternatively activated macrophages

TL;DR: Innate lymphoid type 2 cells maintain eosinophils and alternatively activated macrophages in visceral fat via the production of IL-5 and IL-13.
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Interleukin-4- and Interleukin-13-Mediated Alternatively Activated Macrophages: Roles in Homeostasis and Disease

TL;DR: Recent advances in the understanding of IL-4- and IL-13-mediated alternatively activated macrophages and type 2 immune responses have led to an expanded appreciation for functions of these cells beyond immunity, including maintenance of physiologic homeostasis and tissue repair.
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InterleuKin-33 And Interferon-Γ Counter-Regulate Group 2 Innate Lymphoid Cell Activation During Immune Perturbation

TL;DR: Interleukin-33 mediates activation of ILC2s and Treg cells in resting adipose tissue, but also after helminth infection or treatment with IL-2, and IFN-γ suppresses this pathway, likely to promote inflammatory responses and divert metabolic resources necessary to protect the host.
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Tissue signals imprint ILC2 identity with anticipatory function.

TL;DR: Tissue-specific imprinting dictates the activating receptors ILC2s express, even in germ-free mice, and it is shown that endogenous, tissue-derived signals drive the maturation of I LC2 subsets by controlling expression of distinct patterns of activating receptors, thus anticipating tissue-specific perturbations occurring later in life.