K
Karsten Kretschmer
Researcher at Dresden University of Technology
Publications - 60
Citations - 5542
Karsten Kretschmer is an academic researcher from Dresden University of Technology. The author has contributed to research in topics: FOXP3 & Antigen. The author has an hindex of 29, co-authored 58 publications receiving 5085 citations. Previous affiliations of Karsten Kretschmer include Deutsche Forschungsgemeinschaft & Harvard University.
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Journal ArticleDOI
Inducing and expanding regulatory T cell populations by foreign antigen.
Karsten Kretschmer,Irina Apostolou,Daniel Hawiger,Khashayarsha Khazaie,Michel C. Nussenzweig,Michel C. Nussenzweig,Harald von Boehmer +6 more
TL;DR: The conversion of truly naive CD4+ T cells into suppressor cells expressing Foxp3 is reported by targeting of peptide-agonist ligands to dendritic cells and by analysis of Foxp 3 expression at the level of single cells, showing that conversion was achieved by minute antigen doses with suboptimal dendrite cell activation.
Journal ArticleDOI
DNA methylation controls Foxp3 gene expression.
Julia K. Polansky,Karsten Kretschmer,Karsten Kretschmer,Jennifer Freyer,Stefan Floess,Annette I. Garbe,Annette I. Garbe,Udo Baron,Sven Olek,Alf Hamann,Harald von Boehmer,Jochen Huehn +11 more
TL;DR: It is reported that inhibition of DNA methylation by azacytidine, even in absence of exogenous TGF‐β, not only promoted de novo induction of Foxp3 expression during priming, but also conferred stability of Fox p3 expression upon restimulation.
Journal ArticleDOI
Foxp3 occupancy and regulation of key target genes during T-cell stimulation
Alexander Marson,Karsten Kretschmer,Garrett M. Frampton,Elizabeth S Jacobsen,Julia K. Polansky,Kenzie D MacIsaac,Stuart S. Levine,Ernest Fraenkel,Harald von Boehmer,Richard A. Young +9 more
TL;DR: The predominant, although not exclusive, effect of Foxp3 occupancy is to suppress the activation of target genes on T-cell stimulation, which appears to be crucial for the normal function of Treg cells.
Journal ArticleDOI
Small-molecule RORγt antagonists inhibit T helper 17 cell transcriptional network by divergent mechanisms.
Sheng Xiao,Nir Yosef,Jianfei Yang,Yonghui Wang,Ling Zhou,Chen Zhu,Chuan Wu,Erkan Baloglu,Darby Schmidt,Radha Ramesh,Mercedes Lobera,Mark S. Sundrud,Pei-Yun Tsai,Zhijun Xiang,Jinsong Wang,Yan Xu,Xichen Lin,Karsten Kretschmer,Peter B. Rahl,Richard A. Young,Zhong Zhong,David A. Hafler,Aviv Regev,Shomir Ghosh,Alexander Marson,Vijay K. Kuchroo +25 more
TL;DR: This paper identified three retinoid-related orphan receptor gamma t (RORγt)-specific inhibitors that suppress T helper 17 (Th17) cell responses, including Th17-cell-mediated autoimmune disease.
Journal ArticleDOI
Continuous T Cell Receptor Signals Maintain a Functional Regulatory T Cell Pool
J. Christoph Vahl,Christoph Drees,Klaus Heger,Sylvia Heink,Julius C. Fischer,Jelena Nedjic,Naganari Ohkura,Hiromasa Morikawa,Hendrik Poeck,Sonja Schallenberg,David Rieß,Marco Y. Hein,Thorsten Buch,Bojan Polić,Anne Schönle,Robert Zeiser,Annette Schmitt-Gräff,Karsten Kretschmer,Ludger Klein,Thomas Korn,Shimon Sakaguchi,Marc Schmidt-Supprian +21 more
TL;DR: Genetically ablated the TCR of mature Treg cells in vivo revealed that TCR-induced Treg lineage-defining Foxp3 expression and gene hypomethylation were uncoupled from TCR input in mature TReg cells.