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Peer-reviewedCC BYGlia

CX3CR1 Modulates Migration of Resident Microglia Towards Cortical Laser‐Induced Lesions

  • Jens Wagner1
  • Henrike Antony1
  • Cornelia Hoyer1
  • Kristiina Lundgrén2
  • Rabah Soliymani2
  • Sophie Crux1
  • Lena Christine Justus1
  • Kevin Keppler3,1
  • Julia Steffen1
  • Christian Kurts4
  • Daniel Robert Engel5
  • Jochen Wolfgang Herms3,6
2 more authors
  • Maciej M. Lalowski7,2
  • Martin Fuhrmann1
7 affiliations
  1. 1German Center for Neurodegenerative Diseases (DZNE) Bonn Germany
  2. 2Helsinki Institute of Life Science (HiLIFE), Meilahti Proteomics Unit (MPU) University of Helsinki Helsinki Finland
  3. 3Center of Neuropathology and Prion Research Ludwig Maximilians University Munich Germany
  4. 4Institute of Molecular Medicine and Experimental Immunology, University of Bonn Bonn Germany
  5. 5Institute of Experimental Immunology and Imaging, University Duisburg‐Essen Duisburg Germany
  6. 6German Center for Neurodegenerative Diseases (DZNE) Munich Germany
  7. 7Department of Gene Expression Institute of Molecular Biology and Biotechnology, Faculty of Biology, Adam Mickiewicz University Poznań Poland
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Abstract

Microglia are innate immune cells of the central nervous system (CNS). They extend their processes and migrate toward injuries in vivo. However, how the fractalkine receptor (CX3CR1) influences microglial migration remains unknown. Label-free proteomic profiling predicted changes in Ras homology family (RHO)-signaling activity that hint at dysregulated cytoskeleton signaling in Cx3cr1-deficient murine cortex tissue. To further investigate microglial migration, we carried out two-photon in vivo imaging at 4-h intervals for 72 h after a laser lesion in the cortex. Cx3cr1-deficient microglia showed enhanced migration toward the lesion. Additionally, the length and velocity of microglial fine processes extending toward the lesion were increased in Cx3cr1-deficient microglia. Migration remained unchanged in Ccr2-deficient mice, indicating that monocyte-derived macrophages/microglia did not contribute to microglia accumulation around the lesion. These results demonstrate that CX3CR1 modulates microglia migration toward laser-induced CNS injury. Manipulating microglia migration via the CX3CR1 signaling axis is therefore a potential target for the treatment of CNS injury.

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Cite

BibTeXRIS
BibTeX
@article{wagner2026cx3cr1,
  title = {{CX3CR1 Modulates Migration of Resident Microglia Towards Cortical Laser‐Induced Lesions}},
  author = {Jens Wagner and Henrike Antony and Cornelia Hoyer and Kristiina Lundgrén and Rabah Soliymani and Sophie Crux and Lena Christine Justus and Kevin Keppler and Julia Steffen and Christian Kurts and Daniel Robert Engel and Jochen Wolfgang Herms and Maciej M. Lalowski and Martin Fuhrmann},
  journal = {Glia},
  year = {2026},
  month = aug,
  doi = {10.1002/glia.70207},
  url = {https://doi.org/10.1002/glia.70207},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - CX3CR1 Modulates Migration of Resident Microglia Towards Cortical Laser‐Induced Lesions
AU  - Jens Wagner
AU  - Henrike Antony
AU  - Cornelia Hoyer
AU  - Kristiina Lundgrén
AU  - Rabah Soliymani
AU  - Sophie Crux
AU  - Lena Christine Justus
AU  - Kevin Keppler
AU  - Julia Steffen
AU  - Christian Kurts
AU  - Daniel Robert Engel
AU  - Jochen Wolfgang Herms
AU  - Maciej M. Lalowski
AU  - Martin Fuhrmann
PY  - 2026
DA  - 2026/08/15
JO  - Glia
DO  - 10.1002/glia.70207
UR  - https://doi.org/10.1002/glia.70207
AB  - Microglia are innate immune cells of the central nervous system (CNS). They extend their processes and migrate toward injuries in vivo. However, how the fractalkine receptor (CX3CR1) influences microglial migration remains unknown. Label-free proteomic profiling predicted changes in Ras homology family (RHO)-signaling activity that hint at dysregulated cytoskeleton signaling in Cx3cr1-deficient murine cortex tissue. To further investigate microglial migration, we carried out two-photon in vivo imaging at 4-h intervals for 72 h after a laser lesion in the cortex. Cx3cr1-deficient microglia showed enhanced migration toward the lesion. Additionally, the length and velocity of microglial fine processes extending toward the lesion were increased in Cx3cr1-deficient microglia. Migration remained unchanged in Ccr2-deficient mice, indicating that monocyte-derived macrophages/microglia did not contribute to microglia accumulation around the lesion. These results demonstrate that CX3CR1 modulates microglia migration toward laser-induced CNS injury. Manipulating microglia migration via the CX3CR1 signaling axis is therefore a potential target for the treatment of CNS injury.
SN  - 0894-1491
SN  - 1098-1136
ER  -