Renske L. R. E. Taggenbrock

ORCID: 0000-0003-4165-6877
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About
Contact & Profiles
Research Areas
  • Immune Cell Function and Interaction
  • Genetics and Neurodevelopmental Disorders
  • Alzheimer's disease research and treatments
  • Neurogenesis and neuroplasticity mechanisms
  • IL-33, ST2, and ILC Pathways
  • Monoclonal and Polyclonal Antibodies Research
  • Cell Adhesion Molecules Research
  • Autism Spectrum Disorder Research
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Eosinophilic Esophagitis
  • Immunotherapy and Immune Responses
  • Neurological Disease Mechanisms and Treatments
  • T-cell and B-cell Immunology
  • Cellular Mechanics and Interactions
  • CAR-T cell therapy research
  • Glycosylation and Glycoproteins Research
  • Signaling Pathways in Disease
  • Cancer Immunotherapy and Biomarkers
  • Immunodeficiency and Autoimmune Disorders

University Medical Center Utrecht
2016-2024

Sanquin
2018-2022

Amsterdam University Medical Centers
2021-2022

University of Amsterdam
2021-2022

Janssen (Netherlands)
2018

Johnson & Johnson (Netherlands)
2018

The neuronal cell adhesion molecule contactin-4 ( CNTN4 ) is genetically associated with autism spectrum disorder (ASD) and other psychiatric disorders. Cntn4 -deficient mouse models have previously shown that plays important roles in axon guidance synaptic plasticity the hippocampus. However, pathogenesis functional role of cortex has not yet been investigated. Our study found a reduction cortical thickness motor −/− mice, but migration differentiation were unaffected. Significant...

10.1098/rsob.240018 article EN cc-by Open Biology 2024-05-01

Tissue-resident memory T cells (Trm) are retained in peripheral tissues after infection for enhanced protection against secondary encounter with the same pathogen. We have previously shown that transcription factor Hobit and its homolog Blimp-1 drive Trm development viral infection, but how when these factors mediate formation remains poorly understood. In particular, major impact of regulating several aspects effector T-cell differentiation impairs study specific role development. Here, we...

10.1002/eji.202149665 article EN cc-by-nc-nd European Journal of Immunology 2022-04-07

In view of important neurobiological functions the cell adhesion molecule contactin-6 (Cntn6) that have emerged from studies on null-mutant mice and autism spectrum disorders (ASD) patients, we set out to examine pathways underlying Cntn6 using a proteomics approach. We identified GPCR latrophilin-1 (Lphn1, a.k.a. CIRL1/CL, ADGRL1) as binding partner for forming together heteromeric cis-complex. Lphn1 expression in cultured neurons caused reduction neurite outgrowth increase apoptosis, which...

10.3389/fnmol.2016.00143 article EN cc-by Frontiers in Molecular Neuroscience 2016-12-15

Misfolding and aggregation of tau protein are closely associated with the onset progression Alzheimer's Disease (AD). By interrogating IgG+ memory B cells from asymptomatic donors peptides, we have identified two somatically mutated VH5–51/VL4–1 antibodies. One these, CBTAU-27.1, binds to motif in R3 repeat domain blocks into paired helical filaments (PHFs) by sequestering monomeric tau. The other, CBTAU-28.1, N-terminal insert region inhibits spreading seeds mediates uptake aggregates...

10.1186/s40478-018-0543-z article EN cc-by Acta Neuropathologica Communications 2018-05-31

Abstract iNKT cells are CD1d‐restricted T that play a pro‐inflammatory or regulatory role in infectious and autoimmune diseases. Thymic precursors of eventually develop into distinct iNKT1, iNKT2, iNKT17 lineages the periphery. It remains unclear whether retain developmental potential after lineage commitment. acquire similar phenotype as tissue‐resident memory cells, suggesting they also differentiate along trajectory enables them to persist peripheral tissues. Here, we addressed commitment...

10.1002/eji.202149360 article EN cc-by-nc-nd European Journal of Immunology 2021-12-13

Alzheimer's disease (AD) is a progressive neurodegenerative condition in which aggregated tau and amyloid proteins accumulate the brain causing neuronal dysfunction eventually leads to cognitive decline. Hyperphosphorylated aggregates neuron are believed cause most of pathology associated with AD. These assumed be released into extracellular compartment taken up by adjacent healthy neurons where they induce further aggregation. This "prion-like" spreading can interrupted antibodies capable...

10.3791/58576 article EN Journal of Visualized Experiments 2018-11-09

Abstract The neuronal cell adhesion molecule contactin-4 (CNTN4) has been genetically linked to autism spectrum disorders (ASD) and other psychiatric disorders. Cntn4 -deficient mouse model previously shown that CNTN4 important roles in axon guidance synaptic plasticity the hippocampus. However, pathogenesis functional role of cortex have not yet investigated. Using Nissl staining, immunohistochemistry Golgi staining motor -/- mice was analysed for abnormalities. Interacting partners were...

10.1101/2023.08.25.554833 preprint EN cc-by bioRxiv (Cold Spring Harbor Laboratory) 2023-08-28

ABSTRACT Misfolding and aggregation of tau protein are closely associated with the onset progression Alzheimer’s Disease (AD). By interrogating IgG + memory B cells from asymptomatic donors peptides, we have identified two somatically mutated V H 5-51/V L 4-1 antibodies. One these, CBTAU-27.1, binds to motif in R3 repeat domain blocks into paired helical filaments (PHFs) by sequestering monomeric tau. The other, CBTAU-28.1, N-terminal insert region inhibits spreading seeds mediates uptake...

10.1101/287003 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2018-03-22

Alzheimer's disease (AD) is a progressive neurodegenerative condition in which aggregated tau and amyloid proteins accumulate the brain causing neuronal dysfunction eventually leads to cognitive decline. Hyperphosphorylated aggregates neuron are believed cause most of pathology associated with AD. These assumed be released into extracellular compartment taken up by adjacent healthy neurons where they induce further aggregation. This "prion-like" spreading can interrupted antibodies capable...

10.3791/58576-v article EN Journal of Visualized Experiments 2018-11-09
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