Simon Bornschein

ORCID: 0000-0001-9401-3598
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About
Contact & Profiles
Research Areas
  • Cytokine Signaling Pathways and Interactions
  • Immune Cell Function and Interaction
  • Acute Myeloid Leukemia Research
  • Acute Lymphoblastic Leukemia research
  • CAR-T cell therapy research
  • Chronic Myeloid Leukemia Treatments
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • CRISPR and Genetic Engineering
  • interferon and immune responses
  • HIV Research and Treatment
  • Reproductive System and Pregnancy
  • Systemic Lupus Erythematosus Research
  • Autoimmune and Inflammatory Disorders Research
  • Cancer-related molecular mechanisms research
  • RNA modifications and cancer
  • Lymphoma Diagnosis and Treatment
  • Inflammasome and immune disorders
  • Ocular Diseases and Behçet’s Syndrome
  • Viral Infectious Diseases and Gene Expression in Insects
  • Oral Health Pathology and Treatment
  • Parvovirus B19 Infection Studies
  • IL-33, ST2, and ILC Pathways
  • Adolescent and Pediatric Healthcare
  • Cytomegalovirus and herpesvirus research
  • Immune Response and Inflammation

Celyad (Belgium)
2018-2020

VIB-KU Leuven Center for Cancer Biology
2017-2019

Centro de Investigación Biomédica en Red de Cáncer
2019

Institute for Molecular Medicine Finland
2019

Finland University
2019

University of Helsinki
2019

KU Leuven
2013-2018

VIB-KU Leuven Center for Brain & Disease Research
2018

VIB-KU Leuven Center for Microbiology
2014-2015

Objective To identify the underlying genetic defect in a 16‐year‐old girl with severe early‐onset and refractory systemic lupus erythematosus (SLE), IgA deficiency, mild lower limb spasticity without neuroradiologic manifestations. Methods Whole‐exome sequencing extensive immunologic analysis were performed on samples from index patient. Results We identified de novo p.R779H IFIH1 gain‐of‐function mutation patient SLE, selective spasticity. The same was recently patients Aicardi‐Goutières...

10.1002/art.39110 article EN Arthritis & Rheumatology 2015-03-16

Abstract Leukemia is caused by the accumulation of multiple genomic lesions in hematopoietic precursor cells. However, how these events cooperate during oncogenic transformation remains poorly understood. We studied cooperation between activated JAK3/STAT5 signaling and HOXA9 overexpression, two identified as significantly co-occurring T-cell acute lymphoblastic leukemia. Expression mutant JAK3 led to a rapid development leukemia originating from multipotent or lymphoid-committed...

10.1158/2159-8290.cd-17-0583 article EN Cancer Discovery 2018-03-02

Mutations in the interleukin-7 receptor (IL7R) or Janus kinase 3 (JAK3) occur frequently T-cell acute lymphoblastic leukemia (T-ALL) and both are able to drive cellular transformation development of T-ALL mouse models. However, signal transduction pathways downstream JAK3 mutations remain poorly characterized. Here we describe phosphoproteome JAK3(L857Q)/(M511I) activating transformed Ba/F3 lymphocyte cells. Signaling regulated by mutants were assessed following inhibition JAK1/JAK3 using...

10.1038/leu.2017.276 article EN cc-by-nc-sa Leukemia 2017-08-30

Mammalian genomes encode a plethora of long non-coding RNA (lncRNA). These transcripts are thought to regulate gene expression, influencing biological processes from development pathology. Results the few lncRNA that have been studied in context immune system highlighted potentially critical functions as network regulators. Here we explored nature transcriptome regulatory T cells (Tregs), subset CD4+ required establish and maintain immunological self-tolerance. The identified Treg showed...

10.3389/fimmu.2018.01989 article EN cc-by Frontiers in Immunology 2018-09-25

T-cell acute lymphoblastic leukemia (T-ALL) is caused by the accumulation of multiple mutations combined with ectopic expression transcription factors in developing T cells. However, molecular basis underlying cooperation between factor and additional oncogenic driving T-ALL has been difficult to assess due limited robust model systems. Here we utilize a new ex vivo pro-T-cell study cooperation. Using systems biological approach first dissect signaling network driven interleukin-7, stem cell...

10.1038/leu.2017.328 article EN cc-by-nc-sa Leukemia 2017-11-20

Abstract Mucosa‐associated lymphoid tissue 1 (Malt1) regulates immune cell function by mediating the activation of nuclear factor κB (NF‐κB) signaling through both its adaptor and proteolytic function. Malt1 is also a target own protease activity this self‐cleavage further contributes to NF‐κB activity. Until now, functional distinction between general in regulating remained unclear. Here we demonstrate, using new mouse model, importance expression genes subsequent T activation....

10.1002/eji.201847597 article EN cc-by-nc European Journal of Immunology 2018-07-19

Abstract To fulfill a productive infection cycle the human immunodeficiency virus (HIV) relies on host-cell factors. Interference with these co-factors holds great promise in protecting cells against HIV infection. LEDGF/p75, encoded by PSIP1 gene, is used integrase (IN) protein pre-integration complex of to bind chromatin facilitating proviral integration. LEDGF/p75 depletion results defective replication. However, as part its cellular function tethers proteins genome. We site-specific...

10.1038/s41598-019-38718-0 article EN cc-by Scientific Reports 2019-02-20

<h3>Background</h3> Chimeric antigen receptor (CAR)-T cell therapy, a promising cancer treatment, is expanding its applications to target autoimmune disorders, neurobiology, and ageing. Industry standard CAR-T development relies heavily on i) selecting an antibody based affinity screening ii) high-affinity binders in the context of CAR. However, recent data challenge notion that strongest binder always leads best CAR, revealing low-affinity can enhance activity improve patient...

10.1136/jitc-2024-sitc2024.1220 article EN cc-by-nc Regular and Young Investigator Award Abstracts 2024-11-01

Cell and immunotherapy offer transformative potential for treating diseases like cancer autoimmune disorders by modulating the immune system. The development of these therapies is resource-intensive, with majority drug candidates failing to progress beyond laboratory testing. While recent advances in machine learning have revolutionised areas such as protein engineering, applications remain limited due scarcity large-scale, standardised datasets complexity cellular systems. In this work, we...

10.48550/arxiv.2412.01388 preprint EN arXiv (Cornell University) 2024-12-02

Gain-of-function mutations in IFIH1 were identified Aicardi-Goutieres syndrome (AGS), a rare neuroimmunological disorder associated with elevated levels of type I interferon and characterized by leucoencephalopathy, brain atrophy intracranial calcifications leading to profound intellectual disability, spasticity dystonia. functions as an intracellular innate immune receptor that senses viral nucleic acids leads the induction proinflammatory cytokines.

10.1186/1546-0096-12-s1-p309 article EN cc-by Pediatric Rheumatology 2014-09-01

3103 Background: Engineered T cells expressing chimeric antigen receptors (CAR) are now delivering clinically relevant results in patients with advanced hematological malignancies. One critical area for future development is to modulate gene expression thereby endowing the engineered cell specific desired features that enhance anti-tumor activity. Methods: Short-hairpin RNA (shRNA) were cloned individually or multiplexed within micro-RNA scaffolds enabled co-expression of individual shRNA a...

10.1200/jco.2020.38.15_suppl.3103 article EN Journal of Clinical Oncology 2020-05-20
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