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Nadine Waldschmitt

Researcher at Technische Universität München

Publications -  26
Citations -  3603

Nadine Waldschmitt is an academic researcher from Technische Universität München. The author has contributed to research in topics: Gut flora & Immune system. The author has an hindex of 13, co-authored 22 publications receiving 2492 citations. Previous affiliations of Nadine Waldschmitt include French Institute of Health and Medical Research & university of lille.

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Anticancer immunotherapy by CTLA-4 blockade relies on the gut microbiota

TL;DR: A key role is revealed for Bacteroidales in the immunostimulatory effects of CTLA-4 blockade, which is found to depend on distinct Bacteroides species in mice and patients.
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Enterococcus hirae and Barnesiella intestinihominis Facilitate Cyclophosphamide-Induced Therapeutic Immunomodulatory Effects

TL;DR: Enterococcus hirae and B. intestinihominis represent valuable "oncomicrobiotics" ameliorating the efficacy of the most common alkylating immunomodulatory compound CTX, and selectively predicted longer progression-free survival in advanced lung and ovarian cancer patients treated with chemo-immunotherapy.
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Mitochondrial function controls intestinal epithelial stemness and proliferation

TL;DR: Compensatory hyperproliferation of HSP60+ escaper stem cells suggests paracrine release of WNT-related factors from H SP60-deficient, functionally impaired IEC to be pivotal in the control of the proliferative capacity of the stem cell niche.
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Fine-Tuning Cancer Immunotherapy: Optimizing the Gut Microbiome.

TL;DR: Findings that specific gut-resident bacteria determine the immunotherapeutic responses associated with CTLA-4 checkpoint blockade are presented, and how this new understanding could improve the therapeutic coverage of immune checkpoint inhibitors, and potentially limit their immune-mediated toxicity, through the use of adjunctive "oncomicrobiotics".
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Mitochondrial impairment drives intestinal stem cell transition into dysfunctional Paneth cells predicting Crohn's disease recurrence.

TL;DR: Evidence is provided that inflammation-associated mitochondrial dysfunction in the intestinal epithelium triggers a metabolic imbalance, causing reduced stemness and acquisition of a dysfunctional PC phenotype, and blocking glycolysis might be a novel drug target to antagonise PC dysfunction inThe pathogenesis of CD.