Marina A. Freudenberg
University of Freiburg
147 Papers
2.1K Citations
Marina A. Freudenberg is an academic researcher from University of Freiburg. The author has contributed to research in topics: Innate immune system & TLR4. The author has an hindex of 60, co-authored 147 publications. Previous affiliations of Marina A. Freudenberg include Max Planck Society.
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Papers
Impaired immune and acute-phase responses in interleukin-6-deficient mice
Manfred Kopf,Heinz Baumann,Giulia Freer,Marina A. Freudenberg,Marinus C. Lamers,Tadamitsu Kishimoto,Rolf M. Zinkernagel,Horst Bluethmann,Georges Köhler +8 more
TL;DR: It is concluded that IL-6 production induced by injury or infection is an important in vivo SOS signal which coordinates activities of liver cells, macrophages and lymphocytes.
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Oligosaccharides of Hyaluronan Activate Dendritic Cells via Toll-like Receptor 4
Christian Termeer,Frauke Benedix,Jonathon Sleeman,Christina Fieber,Ursula Voith,Thomas Ahrens,Kensuke Miyake,Marina A. Freudenberg,Christopher Galanos,Jan-Christoph Simon +9 more
TL;DR: This is the first report that polysaccharide degradation products of the extracellular matrix produced during inflammation might serve as an endogenous ligand for the TLR-4 complex on DCs.
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Galactosamine-induced sensitization to the lethal effects of endotoxin.
TL;DR: The data so far suggests that the sensitization to lipopolysaccharide is related only to the early metabolic effects of the hexosamine, which is known to exhibit hepatotoxic activity inducing ultimate necrosis of the hepatocytes.
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CD14 is required for MyD88-independent LPS signaling
Zhengfan Jiang,Philippe Georgel,Xin Du,Louis Shamel,Sosathya Sovath,Suzanne Mudd,Michael Huber,Christoph Kalis,Simone Keck,Chris Galanos,Marina A. Freudenberg,Bruce Beutler +11 more
TL;DR: The recessive mutation 'Heedless' (hdl) was detected in third-generation N-ethyl-N-nitrosourea–mutated mice that showed defective responses to microbial inducers, and the data suggest that the TLR4–MD-2 complex distinguishes LPS chemotypes, but CD14 nullifies this distinction.
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Crucial role for human Toll-like receptor 4 in the development of contact allergy to nickel
Marc Schmidt,Badrinarayanan Raghavan,Badrinarayanan Raghavan,Verena Müller,Verena Müller,Thomas Vogl,György Fejer,Sandrine Tchaptchet,Simone Keck,Christoph Kalis,Peter J. Nielsen,Chris Galanos,Johannes Roth,Arne Skerra,Stefan F. Martin,Marina A. Freudenberg,Matthias Goebeler,Matthias Goebeler +17 more
TL;DR: It is shown that Ni2+ triggered an inflammatory response by directly activating human Toll-like receptor 4 (TLR4), which implicate site-specific human TLR4 inhibition as a potential strategy for therapeutic intervention in CHS that would not affect vital immune responses.
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