Nina Burgdorf

ORCID: 0000-0003-4287-7751
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About
Contact & Profiles
Research Areas
  • Immune Cell Function and Interaction
  • T-cell and B-cell Immunology
  • CAR-T cell therapy research
  • Immunotherapy and Immune Responses
  • RNA modifications and cancer
  • Complement system in diseases
  • IL-33, ST2, and ILC Pathways
  • Cellular transport and secretion
  • Cancer-related gene regulation
  • Lipid Membrane Structure and Behavior
  • Asthma and respiratory diseases
  • RNA and protein synthesis mechanisms
  • interferon and immune responses

Inserm
2018-2024

Institut Curie
2018-2024

Université Paris Sciences et Lettres
2018-2024

Immunité et Cancer
2022-2024

La Ligue Contre le Cancer
2018

Center for Experimental and Clinical Infection Research
2016

Helmholtz Centre for Infection Research
2016

Medizinische Hochschule Hannover
2016

After priming, naïve CD8+ T lymphocytes establish specific heritable transcription programs that define progression to long-lasting memory cells or short-lived effector cells. Although lineage specification is critical for protection, it remains unclear how chromatin dynamics contributes the control of gene expression programs. We explored role silencing by histone methyltransferase Suv39h1. In murine activated after Listeria monocytogenes infection, Suv39h1-dependent trimethylation H3...

10.1126/science.aah6499 article EN Science 2018-01-12

Oncogenesis often implicates epigenetic alterations, including derepression of transposable elements (TEs) and defects in alternative splicing. Here, we explore the possibility that noncanonical splice junctions between exons TEs represent a source tumor-specific antigens. We show mouse normal tissues tumor cell lines express wide but distinct ranges mRNA TEs, some which are specific. Immunopeptidome analyses identified peptides derived from exon-TE splicing associated to MHC-I molecules....

10.1126/sciimmunol.abm6360 article EN Science Immunology 2023-02-03

Naive CD4+ T lymphocytes differentiate into different effector types, including helper and regulatory cells (Th Treg, respectively). Heritable gene expression programs that define these types are established during differentiation, but little is known about the epigenetic mechanisms install maintain programs. Here, we use mice defective for components of heterochromatin-dependent silencing to investigate control cell plasticity. We show that, upon receptor (TCR) engagement, naive TRIM28 (an...

10.1073/pnas.1901639116 article EN cc-by-nc-nd Proceedings of the National Academy of Sciences 2019-11-27

SUMMARY Evidence indicates that transposable elements (TEs) stimulate innate sensing pathways in various pathologies but it is not clear whether they are sensed during normal physiological responses. Here we show that, activation with an exogenous pathogen associated molecular pattern (PAMP), dendritic cells (DCs) epigenetically remodel heterochromatin at TEs by depleting the methyltransferase Suv39h1 and reducing histone-3 lysine-9 trimethylation (H3K9me3). TLR4 signaling activates TE...

10.1101/2021.09.10.457789 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2021-09-11
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