M
Markus Kleinewietfeld
Researcher at University of Hasselt
Publications - 68
Citations - 10440
Markus Kleinewietfeld is an academic researcher from University of Hasselt. The author has contributed to research in topics: Immune system & FOXP3. The author has an hindex of 28, co-authored 58 publications receiving 8460 citations. Previous affiliations of Markus Kleinewietfeld include Dresden University of Technology & Broad Institute.
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Journal ArticleDOI
Genetic and Epigenetic Fine-Mapping of Causal Autoimmune Disease Variants
Kyle Kai-How Farh,Alexander Marson,Jiang Zhu,Markus Kleinewietfeld,William J. Housley,Samantha Beik,Noam Shoresh,Holly Whitton,Russell J.H. Ryan,Alexander A. Shishkin,Meital Hatan,Marlene J. Carrasco-Alfonso,Dita Mayer,C. John Luckey,Nikolaos A. Patsopoulos,Philip L. De Jager,Vijay K. Kuchroo,Charles B. Epstein,Mark J. Daly,David A. Hafler,Bradley E. Bernstein +20 more
TL;DR: A fine-mapping algorithm is developed to identify candidate causal variants for 21 autoimmune diseases from genotyping data, and it is found that most non-coding risk variants, including those that alter gene expression, affect non-canonical sequence determinants not well-explained by current gene regulatory models.
Journal ArticleDOI
Expression of ectonucleotidase CD39 by Foxp3+ Treg cells: hydrolysis of extracellular ATP and immune suppression
Giovanna Borsellino,Markus Kleinewietfeld,Diletta Di Mitri,Alexander Sternjak,Adamo Diamantini,Raffaella Giometto,Sabine Höpner,Diego Centonze,Giorgio Bernardi,Maria Luisa Dell'Acqua,Paolo Maria Rossini,Luca Battistini,Olaf Rötzschke,Kirsten Falk +13 more
TL;DR: In humans CD39 is a marker of a Treg subset likely involved in the control of the inflammatory autoimmune disease and Notably, patients with the remitting/relapsing form of multiple sclerosis have strikingly reduced numbers of CD39(+) Treg cells in the blood.
Journal ArticleDOI
Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells
Markus Kleinewietfeld,Arndt Manzel,Arndt Manzel,Jens Titze,Jens Titze,Heda Kvakan,Nir Yosef,Ralf A. Linker,Dominik N. Müller,Dominik N. Müller,David A. Hafler,David A. Hafler +11 more
TL;DR: It is shown that increased salt concentrations found locally under physiological conditions in vivo markedly boost the induction of murine and human TH17 cells, which display a highly pathogenic and stable phenotype characterized by the upregulation of the pro-inflammatory cytokines GM-CSF, TNF-α and IL-2.
Journal ArticleDOI
Induction and molecular signature of pathogenic TH17 cells
Youjin Lee,Amit Awasthi,Amit Awasthi,Nir Yosef,Nir Yosef,Francisco J. Quintana,Sheng Xiao,Anneli Peters,Chuan Wu,Markus Kleinewietfeld,Sharon R. Kunder,David A. Hafler,Raymond A. Sobel,Aviv Regev,Aviv Regev,Vijay K. Kuchroo +15 more
TL;DR: It is found that the production of TGF-β3 by developing Th17 cells was dependent on IL-23, which together with IL-6 induced very pathogenic TH17 cells, which had a molecular signature that defined pathogenic effector TH 17 cells in autoimmune disease.
Journal ArticleDOI
Salt-responsive gut commensal modulates TH17 axis and disease
Nicola Wilck,Mariana Matus,Sean M. Kearney,Scott W. Olesen,Kristoffer Forslund,Hendrik Bartolomaeus,Stefanie Haase,Anja Mähler,András Balogh,Lajos Markó,Olga Vvedenskaya,Olga Vvedenskaya,Friedrich H. Kleiner,Dmitry Tsvetkov,Dmitry Tsvetkov,Lars Klug,Paul I. Costea,Shinichi Sunagawa,Lisa A. Maier,Natalia Rakova,Natalia Rakova,Valentin Schatz,Patrick Neubert,Christian Frätzer,Alexander Krannich,Maik Gollasch,Maik Gollasch,Diana A. Grohme,Beatriz F. Côrte-Real,Roman G. Gerlach,Marijana Basic,Athanasios Typas,Chuan Wu,Jens Titze,Jonathan Jantsch,Michael Boschmann,Ralf Dechend,Ralf Dechend,Markus Kleinewietfeld,Markus Kleinewietfeld,Stefan Kempa,Peer Bork,Ralf A. Linker,Eric J. Alm,Dominik Müller +44 more
TL;DR: This paper showed that high salt intake affects the gut microbiome in mice, particularly by depleting Lactobacillus murinus, and treatment of mice with L. murinus prevented salt-induced aggravation of actively induced experimental autoimmune encephalomyelitis and salt-sensitive hypertension by modulating T helper 17 (TH17) cells.