Maja Kitic
University of Mainz
4 Papers
7 Citations
Maja Kitic is an academic researcher from University of Mainz. The author has contributed to research in topics: Microglia & Neuroinflammation. The author has an hindex of 3, co-authored 4 publications.
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Papers
Interleukin-1 promotes autoimmune neuroinflammation by suppressing endothelial heme oxygenase-1 at the blood–brain barrier
Judith Hauptmann,Lisa Johann,Federico Marini,Maja Kitic,Elisa Colombo,Ilgiz A. Mufazalov,Martin Krueger,Khalad Karram,Sonja Moos,Sonja Moos,Florian Wanke,Florian Wanke,Florian C. Kurschus,Florian C. Kurschus,Matthias Klein,Silvia Cardoso,Judith Strauß,Subhashini Bolisetty,Fred Lühder,Markus Schwaninger,Harald Binder,Ingo Bechman,Tobias Bopp,Anupam Agarwal,Miguel P. Soares,Tommy Regen,Ari Waisman +26 more
TL;DR: It is found that IL-1 signaling in microglia and astrocytes is redundant for the development of EAE, whereas theIL-1R1 deletion in BBB-ECs markedly ameliorated disease severity, and Mechanistically, this data emphasize a functional crosstalk of BBb-EC IL- 1 signaling and HO-1, controlling the transcription of downstream proinflammatory genes promoting the pathogenesis of autoimmune neuroinflammation.
Novel Microglia Depletion Systems: A Genetic Approach Utilizing Conditional Diphtheria Toxin Receptor Expression and a Pharmacological Model Based on the Blocking of Macrophage Colony-Stimulating Factor 1 Receptor.
TL;DR: Two approaches to ablate microglia are described: an efficient genetic model that utilizing DTRMG mouse line that has diphtheria toxin receptor (DTR) expression regulated by the promoter activity of the fractalkine receptor (CX3CR1) gene, and a pharmacological model that utilizes the blocking of macrophage colony-stimulating factor 1 receptor (CSF-1R) with a blocking antibody.
6
NG2 plays a role in neuroinflammation but is not expressed by immune cells
Maja Kitic,Khalad Karram,Nicole Israel,Nir Yogev,Sonja M. Lacher,Yilang Tang,Hatice Yigit,Jan Bauer,Florian Wanke,Anela Knezovic,Jacqueline Trotter,Florian C. Kurschus,Ari Waisman +12 more
TL;DR: It is likely that after a stronger boost of the immune system, such as varying concentrations of MOG, CFA and/or pertussis toxin, the threshold for the disease onset can be reached also in NG2-deficient mice.
2
NF-κB inducing kinase (NIK) is an essential post-transcriptional regulator of T-cell activation affecting F-actin dynamics and TCR signaling.
Sonja M. Lacher,Christoph Thurm,Ute Distler,Alma N. Mohebiany,Nicole Israel,Maja Kitic,Anna Ebering,Yilang Tang,Matthias Klein,Guido H. Wabnitz,Florian Wanke,Yvonne Samstag,Tobias Bopp,Florian C. Kurschus,Luca Simeoni,Stefan Tenzer,Ari Waisman +16 more
TL;DR: It is found that NIK-deficient T cells were hampered in phosphorylation of Zap70, LAT, AKT, ERK1/2 and PLCγ upon TCR engagement, disclosing a hitherto unknown function of NIK in T-cell priming and differentiation.