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Articles by Sandra Ammann
ERCC6L2 ensures repair fidelity for staggered-end DNA double-strand breaks - Nature Communications
Abstract DNA double-strand breaks (DSBs) both pose threats to genome integrity and are commonly used for genome editing applications. Structural features of DSB ends play key roles in determining DNA repair pathway usage and outcomes during genome editing, but the cellular factors involved in these processes are only partially known.
Targeted gene editing and near-universal cDNA insertion of CYBA and CYBB as a treatment for chronic granulomatous disease - Nature Communications
Abstract Chronic granulomatous disease (CGD) is a severe inborn error of immunity caused by NADPH oxidase defects. Here, we develop CRISPR/Cas9-based gene editing strategies for correction of variants in the CYBA and CYBB genes causing CGD. For X-linked CGD, we also develop a near-universal gene editing strategy by targeted integration of a truncated CYBB cDNA in CD34+ hematopoietic stem and progenitor cells (HSPCs).
Author Correction: IFNγ binding to extracellular matrix prevents fatal systemic toxicity - Nature Immunology
Correction to: Nature Immunology https://doi.org/10.1038/s41590-023-01420-5, published online 2 February 2023. In the version of the article initially published, Anja Schütz (Protein Production & Characterization Core Facility, Max-Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany), who produced the recombinant proteins used in this study, was inadvertently omitted from the author list. This has now been corrected in the PDF and HTML versions of the article.
Elevated monocyte HLA-DR in pediatric secondary hemophagocytic lymphohistiocytosis: a retrospective study
Introduction Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening condition associated with unregulated and deleterious T-lymphocyte and macrophage activation.
Publisher Correction: IFNγ binding to extracellular matrix prevents fatal systemic toxicity - Nature Immunology
Correction to: Nature Immunology https://doi.org/10.1038/s41590-023-01420-5. Published online 2 February 2023. In the version of this article originally published, there was an error in the order of magnitude for the units displayed on the y axes of the Figure 4g HBG (g/dl) panel and Figure 4h Triglycerides (mg/dl) panel, where the units now reading “20, 15, 10, 5, 0” and “200, 150, 100, 50, 0” appeared in error as “2,000, 1,500, 1,000, 500, 0” and “20,000, 15,000, 10,000, 5,000, 0,” respectively.
IFNγ binding to extracellular matrix prevents fatal systemic toxicity - Nature Immunology
Abstract Interferon-γ (IFNγ) is an important mediator of cellular immune responses, but high systemic levels of this cytokine are associated with immunopathology. IFNγ binds to its receptor (IFNγR) and to extracellular matrix (ECM) via four positively charged C-terminal amino acids (KRKR), the ECM-binding domain (EBD). Across evolution, IFNγ is not well conserved, but the EBD is highly conserved, suggesting a critical function.
NK1.1+ innate lymphoid cells in salivary glands inhibit establishment of tissue‐resident memory CD8+ T cells in mice
Short Communication|Basic Kristoffer Weißert Institute for Immunodeficiency, Center for Chronic Immunodeficiency (CCI), University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany Faculty of Biology, Albert‐Ludwigs‐University of Freiburg, Freiburg, Germany these authors contributed equally; Search for more papers by this author Sandra Ammann Institute for Immunodeficiency, Center for Chronic Immunodeficiency (CCI), University Medical Center Freiburg,...
Functional flow cytometry of monocytes for routine diagnosis of innate primary immunodeficiencies
Publication History Published online: September 14, 2019Accepted: September 9, 2019; Received in revised form: September 6, 2019; Received: June 7, 2019;
Hemophagocytic lymphohistiocytosis as presenting manifestation of profound combined immunodeficiency due to an ORAI1 mutation
Publication HistoryPublished online: June 17, 2017Accepted: May 12, 2017; Received in revised form: April 23, 2017; Received: November 22, 2016;
Tyrosine kinase 2 is not limiting human antiviral type III interferon responses
Tyrosine kinase 2 (TYK2) associates with interferon (IFN) alpha receptor, IL-10 receptor (IL-10R) beta and other cytokine receptor subunits for signal transduction, in response to various cytokines including type I and type III interferons, IL-6, IL-10, IL-12 and IL-23. Data on TYK2 dependence on cytokine responses and in vivo consequences of TYK2 deficiency are inconsistent.
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