A5016667606- interferon and immune responses
- Immune Response and Inflammation
- Inflammasome and immune disorders
- Immune Cell Function and Interaction
- Immunotherapy and Immune Responses
- Cancer Immunotherapy and Biomarkers
- Cytokine Signaling Pathways and Interactions
- RNA Research and Splicing
- Chemokine receptors and signaling
- Viral Infections and Vectors
- Heme Oxygenase-1 and Carbon Monoxide
- RNA regulation and disease
- RNA modifications and cancer
- Cell death mechanisms and regulation
- T-cell and B-cell Immunology
- Inflammatory mediators and NSAID effects
- Cytomegalovirus and herpesvirus research
- RNA Interference and Gene Delivery
- CRISPR and Genetic Engineering
- HIV Research and Treatment
- Cancer-related molecular mechanisms research
- RNA and protein synthesis mechanisms
- IL-33, ST2, and ILC Pathways
- Nuclear Structure and Function
- Immune cells in cancer
Ludwig-Maximilians-Universität München
2016-2025
LMU Klinikum
2018-2025
Gene Therapy Laboratory
2025
University Hospital Bonn
2011-2024
Roche (Switzerland)
2024
Max Planck Institute of Biochemistry
2019-2023
University of Bonn
2011-2021
Center for Integrated Protein Science Munich
2016-2020
Institute of Molecular Medicine
2015
Zero to Three
2013
Abstract The IL-1 family cytokines are regulated on transcriptional and posttranscriptional levels. Pattern recognition cytokine receptors control pro-IL-1β transcription whereas inflammasomes regulate the proteolytic processing of pro-IL-1β. NLRP3 inflammasome, however, assembles in response to extracellular ATP, pore-forming toxins, or crystals only presence proinflammatory stimuli. How activation gene by signaling enables remains elusive controversial. In this study, we show that cell...
The structural basis for the distinction of viral RNA from abundant self in cytoplasm virally infected cells is largely unknown. We demonstrated that 5'-triphosphate end generated by polymerases responsible retinoic acid-inducible protein I (RIG-I)-mediated detection molecules. Detection abrogated capping or nucleoside modification RNA, both occurring during posttranscriptional processing eukaryotes. Genomic prepared a negative-strand virus and virus-infected (but not noninfected cells)...
Abstract The Toll-like receptor (TLR)9 is critical for the recognition of immunostimulatory CpG motifs but may cooperate with other TLRs. We analyzed TLR1–10 mRNA expression by using quantitative real-time PCR in highly purified subsets human PBMC and determined sensitivity these to oligodeoxynucleotides (ODN). TLR1 TLR6 were expressed all cell types examined. TLR10 was B cells weakly plasmacytoid dendritic (PDC). High TLR2 characteristic monocytes. PDC marked levels TLR7 TLR9 directly...
The immature plasmacytoid dendritic cell (PDC) is identical with the principal type I IFN-producing upon viral infection. Oligodeoxynucleotides which contain unmethylated CpG motifs (CpG ODN) are recognized by vertebrate immune system. Previously, we described ODN that strongly activate human B cells and blood cells. Here describe distinct CpG-containing oligonucleotide sequences which, in contrast to previously ODN, induced high amounts of IFN-α IFN-β peripheral mononuclear (PBMC)....
Human plasmacytoid dendritic cells (DC) (PDC, CD123+) and myeloid DC (MDC, CD11c+) may be able to discriminate between distinct classes of microbial molecules based on a different pattern Toll-like receptor (TLR) expression. TLR1–TLR9 were examined in purified PDC MDC. TLR9, which is critically involved the recognition CpG motifs mice, was present PDCbut not TLR4, required for response LPS, selectively expressed Consistent with TLR expression, susceptible stimulation by oligodeoxynucleotide...
A common denominator among the multiple damage-inducing agents that ultimately lead to activation of NLRP3 has not yet been identified. Recently, production reactive oxygen species (ROS) suggested act as a event upstream inflammasome machinery. Because de novo translation is an essential step in NLRP3, we investigated role substances inhibit either ROS or its oxidative activity. Although observe unique other known inflammasomes sensitivity inhibition, have found this phenomenon attributable...
Abstract Inflammasomes are multiprotein signaling platforms that form upon sensing microbe- or damage-associated molecular patterns. Upon their formation, caspase-1 is activated, leading to the processing of certain proinflammatory cytokines and initiation a special type cell death, known as pyroptosis. Among inflammasomes, NLRP3 takes on importance because it appears be general sensor stress. Moreover, unlike other inflammasome sensors, activity under additional transcriptional regulation....