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Thomas Hoyler
Researcher at University of Freiburg
Publications - 11
Citations - 3120
Thomas Hoyler is an academic researcher from University of Freiburg. The author has contributed to research in topics: Innate lymphoid cell & Immunology. The author has an hindex of 8, co-authored 8 publications receiving 2708 citations. Previous affiliations of Thomas Hoyler include University of Mainz.
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Journal ArticleDOI
Differentiation of type 1 ILCs from a common progenitor to all helper-like innate lymphoid cell lineages.
Christoph S.N. Klose,Christoph S.N. Klose,Melanie Flach,Melanie Flach,Luisa Möhle,Leif Rogell,Leif Rogell,Leif Rogell,Thomas Hoyler,Thomas Hoyler,Karolina Ebert,Karolina Ebert,Carola Fabiunke,Carola Fabiunke,Dietmar Pfeifer,Veronika Sexl,Diogo Fonseca-Pereira,Rita G. Domingues,Henrique Veiga-Fernandes,Sebastian J. Arnold,Meinrad Busslinger,Ildiko Rita Dunay,Yakup Tanriver,Andreas Diefenbach +23 more
TL;DR: Interestingly, the CHILP differentiated into ILC2 and ILC3 lineages, but not into conventional natural killer cells that have been considered an ILC1 subset, presenting evidence for a new ILC lineage that protects barrier surfaces against intracellular infections.
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The transcription factor GATA-3 controls cell fate and maintenance of type 2 innate lymphoid cells.
Thomas Hoyler,Christoph S.N. Klose,Abdallah Souabni,Adriana Turqueti-Neves,Dietmar Pfeifer,Emma L. Rawlins,David Voehringer,Meinrad Busslinger,Andreas Diefenbach +8 more
TL;DR: It is demonstrated that GATA-3 is essential for ILC2 fate decisions and similarities between the transcriptional programs controlling ILC and T helper cell fates are revealed.
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Regulated Expression of Nuclear Receptor RORγt Confers Distinct Functional Fates to NK Cell Receptor-Expressing RORγt+ Innate Lymphocytes
Cedric Vonarbourg,Arthur Mortha,Viet L. Bui,Viet L. Bui,Pedro P. Hernandez,Pedro P. Hernandez,Elina A. Kiss,Thomas Hoyler,Melanie Flach,Bertram Bengsch,Robert Thimme,Christoph Hölscher,Manfred Hönig,Ulrich Pannicke,Klaus Schwarz,Carl F. Ware,Daniela Finke,Andreas Diefenbach +17 more
TL;DR: Using adoptive transfer of genetically tagged LTi-like cells, it is demonstrated that NKR⁻RORγt(+) innate lymphocytes but not NK cells were direct progenitors to NKR(+)RORγT(+) cells in vivo.
Journal ArticleDOI
A T-bet gradient controls the fate and function of CCR6 − RORγt + innate lymphoid cells
Christoph S.N. Klose,Elina A. Kiss,Vera Schwierzeck,Vera Schwierzeck,Karolina Ebert,Thomas Hoyler,Yannick d’Hargues,Nathalie Göppert,Andrew L. Croxford,Andrew L. Croxford,Ari Waisman,Yakup Tanriver,Yakup Tanriver,Andreas Diefenbach,Andreas Diefenbach +14 more
TL;DR: Evidence is provided that the transcription factor T-bet determines the fate of a distinct lineage of CCR6−RORγt+ ILCs, a type of innate lymphocyte population required for immunity to intestinal infections, which is essential for the release of mucus-forming glycoproteins required to protect the epithelial barrier during Salmonella enterica infection.
Journal ArticleDOI
Transcription factor EBF1 is essential for the maintenance of B cell identity and prevention of alternative fates in committed cells.
Robert Nechanitzky,Duygu Akbas,Stefanie Scherer,Ildiko Györy,Thomas Hoyler,Senthilkumar Ramamoorthy,Andreas Diefenbach,Rudolf Grosschedl +7 more
TL;DR: Ebf1 was conditionally deleted in committed pro-B cells after transfer into alymphoid mice and it was found that those cells converted into innate lymphoid cells (ILCs) and T cells with variable-diversity-joining (VDJ) rearrangements of loci encoding both B cell and T cell antigen receptors.