Prof. Dr. Ellen D. Renner
Academic Career and Research Areas
To improve patient care and disease prevention, Prof. Renner and her team assess the interaction of human immunity with the environment. The research focus is directed to rare primary immunodeficiencies as human model diseases of chronic lung diseases and allergies. Next to the discovery of novel disease patterns such as autosomal recessive hyper-IgE syndrome, now called DOCK8 deficiency, her research is contributing essential to unravel pathomechanisms and the optimization of diagnostic and therapy. The current focus of her translational research, located at Helmholtz Zentrum München, is directed to develop novel therapeutic options such as gene repair and cell replacement therapy. Next to clinical work at the Hochgebirgsklinik Davos, Prof. Renner is now primary taking care of patients with rare primary diseases focused on hyper-IgE syndromes as well as allergies and chronic lung diseases at the TUM Children's Hospital Schwabing.
Prof. Renner went to Medical School at LMU Munich, specialized in Pediatrics at Dr. von Haunersche Kinderspital and obtained the specialization as a consultant immunologist of the German Society of Immunology. Additionally trained at Hôpital Necker in Paris and Children`s Hospital Seattle & University of Washington in Seattle, she spent several years as head of the immunological diagnostic laboratory at Dr. von Hauner's Children's Hospital and directed an independent and successful research group, funded e.g. by the German Research Foundation (DFG). In 2016 she got appointed to the Faculty of Medicine of the TUM.
- Spokesperson, AKPI-Peditaric Immunology, DGfI (since 2013)
- International travel award, AAAAI New Orleans (US) (2010)
- American Academy of Allergy, Asthma and Immunology’s Strategic Training in Allergy Research (ST*AR) Award 2007, San Diego (US) (2007)
- CIS Primary Immunodeficiency Summer School, Miami (US) (2006)
- Research Award Infectious Diseases, Merck (GER) (2003)
Key Publications (all publications)
Eberherr et al. Rescue of STAT3 Function in Hyper-IgE Syndrome Using Adenine Base Editing. CRISPR Journal 2021 Apr;4(2):178-190.doi: 10.1089/crispr.2020.0111.Abstract
Renner ED, Rylaarsdam S, Anover-Sombke S, Rack AL, Reichenbach J, Carey JC, Zhu Q, Jansson AF, Barboza J, Schimke LF, Leppert MF, Getz MM, Seger RA, Hill HR, Belohradsky BH, Torgerson TR, Ochs HD: „Novel signal transducer and activator of transcription 3 (STAT3) mutations, reduced T(H)17 cell numbers, and variably defective STAT3 phosphorylation in hyper-IgE syndrome”. J Allergy Clin Immunol. 2008; 122(1): 181-187.Abstract
Stentzel S, Hagl B, Abel F, Kahl BC, Rack-Hoch A, Bröker BM, Renner ED: "Reduced Immunoglobulin (Ig) G Response to Staphylococcus aureus in STAT3 Hyper-IgE Syndrome". Clin Infect Dis. 2017; 64(9):1279-1282.Abstract
Hill DA, Siracusa MC, Abt MC, Kim BS, Kobuley D, Kubo M, Kambayashi T, LaRosa DF, Renner ED, Orange JS, Bushman FD & Artis D: „Commensal bacterial–derived signals regulate basophil hematopoiesis and allergic inflammation”. Nature Medicine. 2012; 18(4): 538-46.Abstract
Renner ED, Torgerson TR, Rylaarsdam S, Anover-Sombke S, Golob K, LaFlam T, Zhu Q, Ochs HD: “STAT3 mutation in the original patient with Job's syndrome”. N Engl J Med. 2007; 357(16): 1667-8.Abstract