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Matthias Hesse

Researcher at National Institutes of Health

Publications -  9
Citations -  2076

Matthias Hesse is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Arginase & Interleukin 10. The author has an hindex of 9, co-authored 9 publications receiving 1988 citations. Previous affiliations of Matthias Hesse include Max Planck Society.

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Differential Regulation of Nitric Oxide Synthase-2 and Arginase-1 by Type 1/Type 2 Cytokines In Vivo: Granulomatous Pathology Is Shaped by the Pattern of l-Arginine Metabolism

TL;DR: An important regulatory role for the arginase biosynthetic pathway in the regulation of inflammation is revealed and differential activation of Arg-1/NOS-2 is a critical determinant in the pathogenesis of granuloma formation.
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The pathogenesis of schistosomiasis is controlled by cooperating IL-10-producing innate effector and regulatory T cells.

TL;DR: It is shown that IL-10 is generated by both the innate and adaptive immune response following infection, with both sources regulating the development of type-2 immunity, immune-mediated pathology, and survival of the infected host.
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IL-13 Activates a Mechanism of Tissue Fibrosis That Is Completely TGF-β Independent

TL;DR: Several genes, including interstitial collagens, several MMPs, and tissue inhibitors of metalloprotease-1 were up-regulated in TGF-β1−/− mice by IL-13, demonstrating thatIL-13 activates the fibrogenic machinery directly.
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Cutting Edge: Stat6-Dependent Substrate Depletion Regulates Nitric Oxide Production

TL;DR: It is shown that IL-4 and IL-13 regulate NO production through depletion of arginine, the substrate of inducible NO synthase (iNOS), which has implications for understanding the physiological regulation of NO production.
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NOS-2 mediates the protective anti-inflammatory and antifibrotic effects of the Th1-inducing adjuvant, IL-12, in a Th2 model of granulomatous disease

TL;DR: A beneficial role for NOS-2 in the regulation of inflammation is revealed and it is suggested that the ultimate success of Th2-to-Th1 immune deviation strategies will rely on the efficient activation of Nos-2 expression in downstream effector cells.