M
Mathias Heikenwalder
Researcher at German Cancer Research Center
Publications - 305
Citations - 30360
Mathias Heikenwalder is an academic researcher from German Cancer Research Center. The author has contributed to research in topics: Immune system & Cancer. The author has an hindex of 79, co-authored 290 publications receiving 22903 citations. Previous affiliations of Mathias Heikenwalder include Ludwig Maximilian University of Munich & University of Kiel.
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Journal ArticleDOI
Senescence surveillance of pre-malignant hepatocytes limits liver cancer development
Tae-Won Kang,Tetyana Yevsa,Norman Woller,Lisa Hoenicke,Torsten Wuestefeld,Daniel Dauch,Anja Hohmeyer,Marcus Gereke,Ramona Rudalska,Anna Potapova,Marcus Iken,Mihael Vucur,Siegfried Weiss,Mathias Heikenwalder,Mathias Heikenwalder,Sadaf Khan,Jesús Gil,Dunja Bruder,Michael P. Manns,Peter Schirmacher,Frank Tacke,Michael Ott,Tom Luedde,Thomas Longerich,Stefan Kubicka,Lars Zender +25 more
TL;DR: It is shown that oncogene-induced senescence occurs in otherwise normal murine hepatocytes in vivo, and how the cellularsenescence program is involved in tumour immune surveillance by mounting specific immune responses against antigens expressed in pre-malignant senescent cells is illustrated.
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Microglia emerge from erythromyeloid precursors via Pu.1- and Irf8-dependent pathways
Katrin Kierdorf,Daniel Erny,Tobias Goldmann,Victor Sander,Christian Schulz,Elisa Gomez Perdiguero,Peter Wieghofer,Annette Heinrich,Pia Riemke,Christoph Hölscher,Dominik N. Müller,Bruno Luckow,Thomas Brocker,Katharina Debowski,Günter Fritz,Ghislain Opdenakker,Andreas Diefenbach,Knut Biber,Knut Biber,Mathias Heikenwalder,Frederic Geissmann,Frank Rosenbauer,Marco Prinz +22 more
TL;DR: It is found that mouse microglia were derived from primitive c-kit+ erythromyeloid precursors that were detected in the yolk sac as early as 8 d post conception and microgliogenesis was not only dependent on the transcription factor Pu.1, but also required Irf8, which was vital for the development of the A2 population, whereas Myb, Id2, Batf3 and Klf4 were not required.
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Microglia in the adult brain arise from Ly-6ChiCCR2+ monocytes only under defined host conditions
Alexander Mildner,Hauke Schmidt,Mirko Nitsche,Doron Merkler,Uwe-Karsten Hanisch,Matthias Mack,Mathias Heikenwalder,Wolfgang Brück,Josef Priller,Marco Prinz +9 more
TL;DR: Using a panel of bone marrow chimeric and adoptive transfer experiments, it is found that circulating Ly-6ChiCCR2+ monocytes were preferentially recruited to the lesioned brain and differentiated into microglia.
Journal ArticleDOI
The maternal microbiota drives early postnatal innate immune development
Mercedes Gomez de Agüero,Stephanie C. Ganal-Vonarburg,Tobias Fuhrer,Sandra Rupp,Yasuhiro Uchimura,Hai Li,Anna Steinert,Mathias Heikenwalder,Siegfried Hapfelmeier,Uwe Sauer,Kathy D. McCoy,Andrew J. Macpherson +11 more
TL;DR: By transiently colonizing pregnant female mice, it is shown that the maternal microbiota shapes the immune system of the offspring and Pups born to mothers transiently Colonized in pregnancy are better able to avoid inflammatory responses to microbial molecules and penetration of intestinal microbes.
Journal ArticleDOI
Specific and nonhepatotoxic degradation of nuclear hepatitis B virus cccDNA.
Julie Lucifora,Yuchen Xia,Florian Reisinger,Ke Zhang,Daniela Stadler,Xiaoming Cheng,Martin F. Sprinzl,Herwig Koppensteiner,Zuzanna Makowska,Tassilo Volz,Caroline Remouchamps,Wen Min Chou,Wolfgang E. Thasler,Norbert Hüser,David Durantel,T. Jake Liang,Carsten Münk,Markus H. Heim,Jeffrey L. Browning,Emmanuel Dejardin,Maura Dandri,Michael Schindler,Mathias Heikenwalder,Ulrike Protzer +23 more
TL;DR: It is described how interferon-α can induce specific degradation of the nuclear viral DNA without hepatotoxicity and proposed lymphotoxin-β receptor activation as a therapeutic alternative and the development of new therapeutics that, in combination with existing antivirals, may cure hepatitis B.