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Benakis, C.* ; Simats, A.* ; Tritschler, S. ; Heindl, S.* ; Besson-Girard, S.* ; Llovera, G.* ; Pinkham, K.* ; Kolz, A.* ; Ricci, A.* ; Theis, F.J. ; Bittner, S.* ; Gökçe, A.* ; Peters, A.* ; Liesz, A.*

T cells modulate the microglial response to brain ischemia.

eLife 11:e82031 (2022)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Neuroinflammation after stroke is characterized by the activation of resident microglia and the invasion of circulating leukocytes into the brain. Although lymphocytes infiltrate the brain in small number, they have been consistently demonstrated to be the most potent leukocyte subpopulation contributing to secondary inflammatory brain injury. However, the exact mechanism of how this minimal number of lymphocytes can profoundly affect stroke outcome is still largely elusive. Here, using a mouse model for ischemic stroke, we demonstrated that early activation of microglia in response to stroke is differentially regulated by distinct T cell subpopulations - with TH1 cells inducing a type I INF signaling in microglia and regulatory T cells (TREG) cells promoting microglial genes associated with chemotaxis. Acute treatment with engineered T cells overexpressing IL-10 administered into the cisterna magna after stroke induces a switch of microglial gene expression to a profile associated with pro-regenerative functions. Whereas microglia polarization by T cell subsets did not affect the acute development of the infarct volume, these findings substantiate the role of T cells in stroke by polarizing the microglial phenotype. Targeting T cell-microglia interactions can have direct translational relevance for further development of immune-targeted therapies for stroke and other neuroinflammatory conditions.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter T Cells ; Immunology ; Inflammation ; Microglia ; Mouse ; Neuroscience ; Single-cell Transcriptomics ; Stroke; B-cells; Stroke; Neuroinflammation; Differentiation; Inflammation; Mechanisms; Expression; Cytokine; Invasion
Sprache englisch
Veröffentlichungsjahr 2022
HGF-Berichtsjahr 2022
ISSN (print) / ISBN 2050-084X
e-ISSN 2050-084X
Zeitschrift eLife
Quellenangaben Band: 11, Heft: , Seiten: , Artikelnummer: e82031 Supplement: ,
Verlag eLife Sciences Publications
Verlagsort Sheraton House, Castle Park, Cambridge, Cb3 0ax, England
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Computational Biology (ICB)
Institute of Diabetes and Regeneration Research (IDR)
POF Topic(s) 30205 - Bioengineering and Digital Health
30201 - Metabolic Health
Forschungsfeld(er) Enabling and Novel Technologies
Helmholtz Diabetes Center
PSP-Element(e) G-503800-001
G-502300-001
Förderungen European Research Council
DOI 10.7554/eLife.82031
WOS ID 000931389900001
Scopus ID 85144585006
PubMed ID 36512388
Erfassungsdatum 2022-12-20
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