S
Susanne Unger
Researcher at University of Zurich
Publications - 39
Citations - 2000
Susanne Unger is an academic researcher from University of Zurich. The author has contributed to research in topics: Common variable immunodeficiency & Immune system. The author has an hindex of 15, co-authored 30 publications receiving 1244 citations. Previous affiliations of Susanne Unger include University Medical Center Freiburg & University of Freiburg.
Papers
More filters
Journal ArticleDOI
Autosomal dominant immune dysregulation syndrome in humans with CTLA4 mutations.
Desirée Schubert,Desirée Schubert,Claudia Bode,Rupert Kenefeck,Tie Zheng Hou,James B. Wing,Alan Kennedy,Alla Bulashevska,Britt-Sabina Petersen,Alejandro A. Schäffer,Björn Grüning,Susanne Unger,Natalie Frede,Ulrich Baumann,Torsten Witte,Reinhold E. Schmidt,G Dueckers,Tim Niehues,Suranjith L. Seneviratne,Maria Kanariou,Carsten Speckmann,Stephan Ehl,Anne Rensing-Ehl,Klaus Warnatz,Mirzokhid Rakhmanov,Robert Thimme,Peter Hasselblatt,Florian Emmerich,Toni Cathomen,Rolf Backofen,Paul Fisch,Maximilian Seidl,Annette M. May,Annette Schmitt-Graeff,Shinji Ikemizu,Ulrich Salzer,Andre Franke,Shimon Sakaguchi,Lucy S. K. Walker,David M. Sansom,Bodo Grimbacher +40 more
TL;DR: Taking together, mutations in CTLA4 resulting inCTLA-4 haploinsufficiency or impaired ligand binding result in disrupted T and B cell homeostasis and a complex immune dysregulation syndrome.
Journal ArticleDOI
Single-Cell Mapping of Human Brain Cancer Reveals Tumor-Specific Instruction of Tissue-Invading Leukocytes.
Ekaterina Friebel,Konstantina Kapolou,Susanne Unger,Nicolás Gonzalo Núñez,Sebastian G. Utz,Elisabeth J. Rushing,Luca Regli,Michael Weller,Melanie Greter,Sonia Tugues,Marian Christoph Neidert,Burkhard Becher +11 more
TL;DR: This work has mapped the leukocyte landscape of brain tumors using high-dimensional single-cell profiling (CyTOF) and found that tissue-invading TAMs showed a distinctive signature trajectory, revealing tumor-driven instruction along with contrasting lymphocyte activation and exhaustion.
Journal ArticleDOI
The TH1 phenotype of follicular helper T cells indicates an IFN-γ-associated immune dysregulation in patients with CD21low common variable immunodeficiency.
Susanne Unger,Maximilian Seidl,Maximilian Seidl,Pauline A. van Schouwenburg,Mirzokhid Rakhmanov,Alla Bulashevska,Natalie Frede,Bodo Grimbacher,Jens Pfeiffer,Klaudia Schrenk,Klaudia Schrenk,Luis E. Muñoz,Leif G. Hanitsch,Ina Stumpf,Fabian M.P. Kaiser,Oliver Hausmann,Florian Kollert,Sigune Goldacker,Mirjam van der Burg,Baerbel Keller,Klaus Warnatz +20 more
TL;DR: Identification of excessive IFN‐&ggr; production by blood and lymph node–derived T cells of patients with CVID with immune dysregulation will offer new therapeutic avenues for this subgroup.
Journal ArticleDOI
Oncogenic KrasG12D causes myeloproliferation via NLRP3 inflammasome activation
Shaima’a Hamarsheh,Lena Osswald,Benedikt S. Saller,Benedikt S. Saller,Susanne Unger,Donatella De Feo,Janaki Manoja Vinnakota,Martina Konantz,Franziska M. Uhl,Heiko Becker,Michael Lübbert,Khalid Shoumariyeh,Christoph Schürch,Geoffroy Andrieux,Nils Venhoff,Annette Schmitt-Graeff,Sandra Duquesne,Dietmar Pfeifer,Mark E. Cooper,Claudia Lengerke,Melanie Boerries,Melanie Boerries,Justus Duyster,Justus Duyster,Charlotte M. Niemeyer,Charlotte M. Niemeyer,Charlotte M. Niemeyer,Miriam Erlacher,Miriam Erlacher,Miriam Erlacher,Bruce R. Blazar,Burkhard Becher,Olaf Groß,Olaf Groß,Tilman Brummer,Robert Zeiser +35 more
TL;DR: It is shown in patient cells and in mice that oncogenic K-Ras activatesNLRP3 inflammasome to drive myeloproliferation, which can be reversed by genetic or pharmacologic NLRP3 blockade, which paves the way for a therapeutic approach based on immune modulation via NL RP3 blockade in KRAS-mutant myeloid malignancies.
Journal ArticleDOI
Clinical and Immunological Phenotype of Patients With Primary Immunodeficiency Due to Damaging Mutations in NFKB2
Christian Klemann,Christian Klemann,Nadezhda Camacho-Ordonez,Linlin Yang,Zoya Eskandarian,Jessica Rojas-Restrepo,Natalie Frede,Alla Bulashevska,Maximilian Heeg,Moudjahed Saleh Al-Ddafari,Julian Premm,Maximilian Seidl,Sandra Ammann,Sandra Ammann,Roya Sherkat,Nita Radhakrishnan,Klaus Warnatz,Susanne Unger,Robin Kobbe,Anja Hüfner,T. Ronan Leahy,Winnie Ip,Winnie Ip,Siobhan O. Burns,Siobhan O. Burns,Manfred Fliegauf,Bodo Grimbacher +26 more
TL;DR: It is concluded that heterozygous damaging mutations in NFKB2 represent a distinct PID entity exceeding the usual clinical spectrum of CVID and thus causes a heterogeneous, more severe form of PID phenotype with early-onset.