Journal Article

DZNE-2026-00411

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Microglia-glioblastoma crosstalk mediates glioblastoma invasion at the far infiltration zone.

Nebeling, F. C.DZNE* ; Fuhrmann, F.DZNE* ; Mittag, M.DZNE* ; Musacchio, F.DZNE* ; Antony, H.DZNE* ; Gockel, N.DZNE* ; Friker, L. L. ; Leonardelli, S. ; Filser, S.DZNE* ; A, D.DZNE* ; Stork, M.DZNE* ; Bano, D.DZNE* ; Pietsch, T.Extern* ; Giordano, F. A. ; Zhou, Q.DZNE* ; Parrinello, S. ; Hölzel, M. ; Herrlinger, U. ; Salomoni, P.DZNE* ; Fuhrmann, M. (Last author)DZNE*

2026
Cell Press [Cambridge, Mass.]

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Please use a persistent id in citations: doi:10.1016/j.immuni.2026.03.010

Abstract: Glioblastoma (GB) cells infiltrate the brain parenchyma and colonize distant regions, driving recurrence and therapy resistance. Here, we examined dynamic microglial responses to infiltrating tumor cells during GB progression. Three-photon imaging in an autochthonous, immunocompetent GB mouse model enabled visualization of microglia-GB interactions at the far infiltration zone (FIZ) in the corpus callosum (CC). GB infiltration speed varied by anatomical location and tumor microtube (TM) number. Microglia increased surveillance in sparsely infiltrated areas but reduced it with higher GB density, revealing a biphasic response. Directional migration toward GB cells was restricted to microglial subsets within a defined spatial range, indicating heterogeneous reactivity. CX3CR1 deficiency enhanced microglial reactivity while limiting GB cell migration. Microglia depletion with the CSF1R inhibitor PLX5622 reduced GB cell migration and constrained TM plasticity. Thus, microglia respond to GB cell infiltration in a stage-dependent manner and critically modulate dissemination at the FIZ.

Keyword(s): Microglia: pathology (MeSH) ; Microglia: metabolism (MeSH) ; Microglia: immunology (MeSH) ; Animals (MeSH) ; Glioblastoma: pathology (MeSH) ; Glioblastoma: immunology (MeSH) ; Glioblastoma: metabolism (MeSH) ; Mice (MeSH) ; Cell Movement (MeSH) ; Brain Neoplasms: pathology (MeSH) ; Brain Neoplasms: immunology (MeSH) ; Brain Neoplasms: metabolism (MeSH) ; Neoplasm Invasiveness (MeSH) ; Humans (MeSH) ; CX3C Chemokine Receptor 1: genetics (MeSH) ; CX3C Chemokine Receptor 1: metabolism (MeSH) ; Disease Models, Animal (MeSH) ; Cell Line, Tumor (MeSH) ; Corpus Callosum: pathology (MeSH) ; Mice, Inbred C57BL (MeSH) ; Organic Chemicals (MeSH) ; CSF1R inhibition ; CX3CR1-deficiency ; Corpus callosum ; autochthonous mouse model ; diffuse infiltration ; glioblastoma ; microglia ; migration ; motility ; three-photon microscopy ; tumor microtubes ; CX3C Chemokine Receptor 1 ; PLX5622 ; Cx3cr1 protein, mouse ; Organic Chemicals

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Contributing Institute(s):

1. Neuroimmunology and Imaging (AG Fuhrmann)
2. Nuclear Function in CNS Pathophysiology (AG Salomoni)
3. Adaptive Immunity in Neurodegeneration (AG Zhou)
4. Light Microscopy Facility (CRFS-LMF) (LMF)
5. Aging and Neurodegeneration (AG Bano)

Research Program(s):

1. 352 - Disease Mechanisms (POF4-352) (POF4-352)
2. 351 - Brain Function (POF4-351) (POF4-351)
3. 899 - ohne Topic (POF4-899) (POF4-899)

Experiment(s):

1. Light Microscope Facility (CRFS-LMF) / Bonn

Appears in the scientific report 2026

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Database coverage:
; ; ; BIOSIS Previews ; Biological Abstracts ; Clarivate Analytics Master Journal List ; Current Contents - Life Sciences ; Ebsco Academic Search ; Essential Science Indicators ; IF >= 30 ; JCR ; Nationallizenz ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection

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