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Anja Wegner
Researcher at University of Bristol
Publications - 8
Citations - 746
Anja Wegner is an academic researcher from University of Bristol. The author has contributed to research in topics: Immunotherapy & Microglia. The author has an hindex of 7, co-authored 8 publications receiving 656 citations. Previous affiliations of Anja Wegner include Charité & University College London.
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Journal ArticleDOI
Inhibition of IL-12/IL-23 signaling reduces Alzheimer's disease–like pathology and cognitive decline
Johannes vom Berg,Stefan Prokop,Kelly R. Miller,Juliane Obst,Roland E. Kälin,Ileana Lopategui-Cabezas,Ileana Lopategui-Cabezas,Anja Wegner,Florian Mair,Carola G. Schipke,Oliver Peters,York Winter,Burkhard Becher,Frank L. Heppner +13 more
TL;DR: In conclusion, intracerebroventricular delivery of antibodies to p40 significantly reduced the concentration of soluble Aβ species and reversed cognitive deficits in aged APPPS1 mice, suggesting that inhibition of the IL-12/IL-23 pathway may attenuate Alzheimer's disease pathology and cognitive deficits.
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Neuroprotective function for ramified microglia in hippocampal excitotoxicity.
Jonathan Vinet,Hilmar R. J. van Weering,Annette Heinrich,Roland E. Kälin,Anja Wegner,Nieske Brouwer,Frank L. Heppner,Nico van Rooijen,Hendrikus Boddeke,Knut Biber,Knut Biber +10 more
TL;DR: The data strongly suggest that ramified microglia not only screen their microenvironment but additionally protect hippocampal neurons under pathological conditions, and Morphological activation of ramification is thus not required to influence neuronal survival.
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Impact of peripheral myeloid cells on amyloid-β pathology in Alzheimer's disease-like mice.
Stefan Prokop,Kelly R. Miller,Natalia Drost,Susann Handrick,Vidhu Mathur,Vidhu Mathur,Jian Luo,Jian Luo,Anja Wegner,Tony Wyss-Coray,Tony Wyss-Coray,Frank L. Heppner +11 more
TL;DR: It is demonstrated that conditional ablation of resident microglia in a mouse model of Alzheimer’s disease results in no significant change in amyloid-β burden, despite nearly complete replacement with peripheral myeloid cells.
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Myeloid-derived suppressor cells mediate tolerance induction in autoimmune disease.
TL;DR: Increased numbers of tolerogenic PMN‐MDSCs were demonstrated to provide protection from disease in a model of experimental autoimmune encephalomyelitis and adopt a more suppressive phenotype during peptide immunotherapy and inhibit CD4+ T‐cell proliferation in a cell‐contact‐dependent manner.
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Extra-thymically induced T regulatory cell subsets: the optimal target for antigen-specific immunotherapy.
TL;DR: Two main types of inducible Treg cells, interleukin‐10‐secreting or Foxp3+, have now been described, each with distinct characteristics and methods of therapeutic induction, and it is crucial to identify the suitability of either subset in the control of specific immune disorders.