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    Regulatory T cells accumulate and proliferate in the ischemic hemisphere for up to 30 days after MCAO (2013)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Stubbe, Tobias
    Ebner, Friederike (WE 6)
    Richter, Daniel
    Engel, Odilo
    Randolf Engel, Odilo
    Klehmet, Juliane
    Royl, Georg
    Meisel, Andreas
    Nitsch, Robert
    Meisel, Christian
    Brandt, Christine
    Quelle
    Journal of cerebral blood flow and metabolism; 33(1) — S. 37–47
    ISSN: 0271-678x
    Sprache
    Englisch
    Verweise
    DOI: 10.1038/jcbfm.2012.128
    Pubmed: 22968321
    Kontakt
    Institut für Immunologie und Molekularbiologie

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    Gebäude 35
    14163 Berlin
    Tel.+49 30 838 - 518 34 Fax.+49 30 838 451 834

    Abstract / Zusammenfassung

    Local and peripheral immune responses are activated after ischemic stroke. In our present study, we investigated the temporal distribution, location, induction, and function of regulatory T cells (Tregs) and the possible involvement of microglia, macrophages, and dendritic cells after middle cerebral artery occlusion (MCAO). C57BL/6J and Foxp3(EGFP) transgenic mice were subjected to 30 minutes MCAO. On days 7, 14, and 30 after MCAO, Tregs and antigen presenting cells were analyzed using fluorescence activated cell sorting multicolor staining and immunohistochemistry. A strong accumulation of Tregs was observed on days 14 and 30 in the ischemic hemisphere accompanied by the elevated presence and activation of microglia. Dendritic cells and macrophages were found on each analyzed day. About 60% of Foxp3(+) Tregs in ischemic hemispheres were positive for the proliferation marker Ki-67 on days 7 and 14 after MCAO. The transfer of naive CD4(+) cells depleted of Foxp3(+) Tregs into RAG1(-/-) mice 1 day before MCAO did not lead to a de novo generation of Tregs 14 days after surgery. After depletion of CD25(+) Tregs, no changes regarding neurologic outcome were detected. The sustained presence of Tregs in the brain after MCAO indicates a long-lasting immunological alteration and involvement of brain cells in immunoregulatory mechanisms.