David Andruszewski

ORCID: 0000-0003-3645-1877
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About
Contact & Profiles
Research Areas
  • Immune Cell Function and Interaction
  • Immune Response and Inflammation
  • Cytokine Signaling Pathways and Interactions
  • Reproductive System and Pregnancy
  • NF-κB Signaling Pathways
  • Medicinal Plant Pharmacodynamics Research
  • Family Support in Illness
  • T-cell and B-cell Immunology
  • Immunotherapy and Immune Responses
  • Epigenetics and DNA Methylation
  • Genetic Syndromes and Imprinting
  • Breastfeeding Practices and Influences

University Medical Center of the Johannes Gutenberg University Mainz
2017-2024

Johannes Gutenberg University Mainz
2017-2024

Significance In spite of TNF involvement in the pathogenesis multiple sclerosis (MS), systemic neutralization MS patients was not successful. One possible reasons is that possesses both pathogenic and protective features may be related to TNFR1 versus TNFR2 receptor engagement. This study uncovers one such functions mediated by intrinsic signaling T reg cells. mice bearing humanized genetic loci, ablation restricted cells led reduced capacity control Th17 cell responses, exacerbated...

10.1073/pnas.1807499115 article EN cc-by-nc-nd Proceedings of the National Academy of Sciences 2018-11-29

The function of NF‐κB family members is controlled by multiple mechanisms including the transcriptional regulator Bcl‐3, an atypical member IκB family. By using a murine model conditional Bcl‐3 overexpression specifically in T cells, we observed impairment development Th2, Th1, and Th17 cells. High expression promoted CD4 + T‐cell survival, but at same time suppressed proliferation response to TCR stimulation, resulting reduced expansion. As consequence, T‐cell‐specific led inflammation...

10.1002/eji.201746933 article EN European Journal of Immunology 2017-06-09

IL-6 binds to the IL-6R α-chain (IL-6Rα) and signals via signal transducer gp130. Recently, was found also bind cell surface glycoprotein CD5, which would then engage gp130 in absence of IL-6Rα. However, biological relevance this alternative pathway is under debate. In study, we developed a mouse model, murine overexpressed CD11c-Cre-dependent manner. Transgenic mice lethal immune dysregulation syndrome with increased numbers Ly-6G+ neutrophils Ly-6Chi monocytes/macrophages. overexpression...

10.4049/jimmunol.1900876 article EN The Journal of Immunology 2020-01-10

Prenatal imprinting to interleukin 17A (IL-17A) triggers behavioral disorders in offspring. However, reported models of maternal immune activation utilizing immunostimulants, lack specificity elucidate the anatomical compartments IL-17A's action and distinct disturbances it causes. By combining transgenic IL-17A overexpression with deficiency its receptor, we established a novel model prenatal (acronym: PRIMA-17 model). This allowed us study exclusively through embryo-restricted responses....

10.1038/s41380-024-02772-6 article EN cc-by Molecular Psychiatry 2024-10-10

Abstract Prenatal imprinting to interleukin 17A (IL-17A) triggers behavioral disorders in offspring. However, reported models of maternal immune activation utilizing immunostimulants, lack specificity elucidate the anatomical compartments IL-17A’s action and distinct disturbances it causes. By combining transgenic IL-17A overexpression with deficiency its receptor, we established a novel model prenatal (acronym: PRIMA-17 model). This allowed us study exclusively through embryo-restricted...

10.1101/2023.12.25.573296 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2023-12-25

Abstract IL-6 is a pleiotropic cytokine that regulates development and function of variety immune cells. Here we used novel mouse strain in which can be overexpressed Cre-dependent manner show mice with CD11c-Cre mediated overexpression succumb from systemic inflammation. High levels perturbed B T cell primary lymphoid organs, bone marrow thymus. Interestingly, IL-6-triggered inflammation promoted expansion both Th17 Treg cells, two types known for their reciprocal developmental...

10.4049/jimmunol.202.supp.181.4 article EN The Journal of Immunology 2019-05-01
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