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8 results on '"Lutz, Konstantin"'

2. CCL17 Promotes Colitis-Associated Tumorigenesis Dependent on the Microbiota

Author

Metzger, Rebecca, primary, Winter, Lis, additional, Bouznad, Nassim, additional, Garzetti, Debora, additional, von Armansperg, Benedikt, additional, Rokavec, Matjaz, additional, Lutz, Konstantin, additional, Schäfer, Yvonne, additional, Krebs, Sabrina, additional, Winheim, Elena, additional, Friedrich, Verena, additional, Matzek, Dana, additional, Öllinger, Rupert, additional, Rad, Roland, additional, Stecher, Bärbel, additional, Hermeking, Heiko, additional, Brocker, Thomas, additional, and Krug, Anne B., additional

Published
2022
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3. Binding of phosphatidylserine‐positive microparticles by PBMCs classifies disease severity in COVID‐19 patients

Author

Rausch, Lisa, primary, Lutz, Konstantin, additional, Schifferer, Martina, additional, Winheim, Elena, additional, Gruber, Rudi, additional, Oesterhaus, Elina F., additional, Rinke, Linus, additional, Hellmuth, Johannes C., additional, Scherer, Clemens, additional, Muenchhoff, Maximilian, additional, Mandel, Christopher, additional, Bergwelt‐Baildon, Michael, additional, Simons, Mikael, additional, Straub, Tobias, additional, Krug, Anne B., additional, Kranich, Jan, additional, and Brocker, Thomas, additional

Published
2021
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4. Impaired function and delayed regeneration of dendritic cells in COVID-19

Author

Winheim, Elena, primary, Rinke, Linus, additional, Lutz, Konstantin, additional, Reischer, Anna, additional, Leutbecher, Alexandra, additional, Wolfram, Lina, additional, Rausch, Lisa, additional, Kranich, Jan, additional, Wratil, Paul R., additional, Huber, Johanna E., additional, Baumjohann, Dirk, additional, Rothenfusser, Simon, additional, Schubert, Benjamin, additional, Hilgendorff, Anne, additional, Hellmuth, Johannes C., additional, Scherer, Clemens, additional, Muenchhoff, Maximilian, additional, von Bergwelt-Baildon, Michael, additional, Stark, Konstantin, additional, Straub, Tobias, additional, Brocker, Thomas, additional, Keppler, Oliver T., additional, Subklewe, Marion, additional, and Krug, Anne B., additional

Published
2021
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6. Ly6D+Siglec-H+ precursors contribute to conventional dendritic cells via a Zbtb46+Ly6D+ intermediary stage.

Author

Lutz, Konstantin, Musumeci, Andrea, Sie, Christopher, Dursun, Ezgi, Winheim, Elena, Bagnoli, Johannes, Ziegenhain, Christoph, Rausch, Lisa, Bergen, Volker, Luecken, Malte D., Oostendorp, Robert A. J., Schraml, Barbara U., Theis, Fabian J., Enard, Wolfgang, Korn, Thomas, and Krug, Anne B.

Subjects
BONE marrow cells, CELL analysis, PROGENITOR cells, BONE marrow, CELL division, DENDRITIC cells
Abstract

Plasmacytoid and conventional dendritic cells (pDC and cDC) are generated from progenitor cells in the bone marrow and commitment to pDCs or cDC subtypes may occur in earlier and later progenitor stages. Cells within the CD11c+MHCII−/loSiglec-H+CCR9lo DC precursor fraction of the mouse bone marrow generate both pDCs and cDCs. Here we investigate the heterogeneity and commitment of subsets in this compartment by single-cell transcriptomics and high-dimensional flow cytometry combined with cell fate analysis: Within the CD11c+MHCII−/loSiglec-H+CCR9lo DC precursor pool cells expressing high levels of Ly6D and lacking expression of transcription factor Zbtb46 contain CCR9loB220hi immediate pDC precursors and CCR9loB220lo (lo-lo) cells which still generate pDCs and cDCs in vitro and in vivo under steady state conditions. cDC-primed cells within the Ly6DhiZbtb46– lo-lo precursors rapidly upregulate Zbtb46 and pass through a Zbtb46+Ly6D+ intermediate stage before acquiring cDC phenotype after cell division. Type I IFN stimulation limits cDC and promotes pDC output from this precursor fraction by arresting cDC-primed cells in the Zbtb46+Ly6D+ stage preventing their expansion and differentiation into cDCs. Modulation of pDC versus cDC output from precursors by external factors may allow for adaptation of DC subset composition at later differentiation stages. The ontogeny of conventional and plasmacytoid dendritic cells (DC) and how these two cell types are related is not fully known. Here the authors identify a pool of bone marrow precursor cells expressing Ly6D Siglec-H and Zbtb46 that can differentiate into either cDC or pDC and show that type I IFN can limit cDC and favor pDC output from these precursors. [ABSTRACT FROM AUTHOR]

Published
2022
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8. Aquaporin 11, a regulator of water efflux at retinal Müller glial cell surface decreases concomitant with immune-mediated gliosis

Author

Deeg, Cornelia A., Amann, Barbara, Lutz, Konstantin, Hirmer, Sieglinde, Lutterberg, Karina, Kremmer, Elisabeth, and Hauck, Stefanie M.

Subjects
Autoimmune uveitis, Research, Immunology, Blotting, Western, Ependymoglial Cells, Water efflux, Retinal inflammation, Water channel, Aquaporins, AQP4, Immunohistochemistry, AQP5, Autoimmune Diseases, Uveitis, Cellular and Molecular Neuroscience, Neurology, Osmotic Pressure, Animals, Aqp11, Aqp4, Aqp5, Autoimmune Uveitis, Cell Volume Regulation, Retinal Inflammation, Superaquaporin, Water Channel, Water Efflux, Horse Diseases, Cell volume regulation, Gliosis, Horses, AQP11
Abstract

BACKGROUND: Müller glial cells are important regulators of physiological function of retina. In a model disease of retinal inflammation and spontaneous recurrent uveitis in horses (ERU), we could show that retinal Müller glial cells significantly change potassium and water channel protein expression during autoimmune pathogenesis. The most significantly changed channel protein in neuroinflammatory ERU was aquaporin 11 (AQP11). Aquaporins (AQP, 13 members) are important regulators of water and small solute transport through membranes. AQP11 is an unorthodox member of this family and was assigned to a third group of AQPs because of its difference in amino acid sequence (conserved sequence is only 11%) and especially its largely unknown function. METHODS: In order to gain insight into the distribution, localization, and function of AQP11 in the retina, we first developed a novel monoclonal antibody for AQP11 enabling quantification, localization, and functional studies. RESULTS: In the horse retina, AQP11 was exclusively expressed at Müller glial cell membranes. In uveitic condition, AQP11 disappeared from gliotic Müller cells concomitant with glutamine synthase. Since function of AQP11 is still under debate, we assessed the impact of AQP11 channel on cell volume regulation of primary Müller glial cells under different osmotic conditions. We conclude a concomitant role for AQP11 with AQP4 in water efflux from these glial cells, which is disturbed in ERU. This could probably contribute to swelling and subsequent severe complication of retinal edema through impaired intracellular fluid regulation. CONCLUSIONS: Therefore, AQP11 is important for physiological Müller glia function and the expression pattern and function of this water channel seems to have distinct functions in central nervous system. The significant reduction in neuroinflammation points to a crucial role in pathogenesis of autoimmune uveitis.

Published
2016

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