Judith Friesenhagen

Publications9
h-index8
Citations336
Highly Influential Citations10
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Highly pathogenic avian influenza viruses inhibit effective immune responses of human blood‐derived macrophages
TLDR
The data provide first evidences for a strategy of how HPAIVs avoid initial inflammatory responses of macrophages facilitating virus spreading and progression to the systemic stage of disease.
S100-alarmin-induced innate immune programming protects newborn infants from sepsis
TLDR
It is suggested that neonates are characterized by a selective, transient microbial unresponsiveness that prevents harmful hyperinflammation in the delicate neonate while allowing for sufficient immunological protection.
Alarmins MRP8 and MRP14 induce stress tolerance in phagocytes under sterile inflammatory conditions.
H5N1 Virus Activates Signaling Pathways in Human Endothelial Cells Resulting in a Specific Imbalanced Inflammatory Response
TLDR
Defining signaling patterns specifically activated by H5N1, which, in contrast to low pathogenic influenza viruses, are responsible for an imbalance of an overwhelming proinflammatory and impaired antiviral gene program is described.
TNF phase III signalling in tolerant cells is tightly controlled by A20 and CYLD.
In neonates S100A8/S100A9 alarmins prevent the expansion of a specific inflammatory monocyte population promoting septic shock
TLDR
The data suggest that a specific population of inflammatory monocytes promotes fatal courses of sepsis in neonates if its expansion is not regulated by S100A8/S100A9 alarmins, which are associated with hyperinflammatory responses during endotoxemia and fatal septic courses.
C/EBPβ-LAP*/LAP Expression Is Mediated by RSK/eIF4B-Dependent Signalling and Boosted by Increased Protein Stability in Models of Monocytic Differentiation
TLDR
The switch from mTOR- to RSK-mediated signalling to orchestrate eIF4B-dependent LAP*/LAP translation, accompanied by increased protein stability but only small mRNA changes, may be a prototypical example for the regulation of protein expression during selected processes of differentiation/proliferation.
Highly Pathogenic Influenza Viruses Inhibit Inflammatory Response in Monocytes via Activation of Rar-Related Orphan Receptor RORa
TLDR
A novel RORa-dependent escape mechanism by which H5N1 prevents an effective inflammatory response of monocytes blocking NF-κB-dependent gene expression is revealed.
Corrigendum: S100-alarmin-induced innate immune programming protects newborn infants from sepsis
TLDR
In the version of this article initially published, the graphs in Figure 2e were incorrect and have been replaced with the correct graphs.