Publikationsdatenbank

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

Klehmet, Juliane

Royl, Georg

Meisel, Andreas

Nitsch, Robert

Meisel, Christian

Brandt, Christine

Quelle

Journal of cerebral blood flow and metabolism

Bandzählung: 33

Heftzählung: 1

Seiten: 37 – 47

ISSN: 0271-678x

Sprache

Englisch

Verweise

DOI: 10.1038/jcbfm.2012.128

Pubmed: 22968321

Kontakt

Institut für Immunologie

Robert-von-Ostertag-Str. 7-13
14163 Berlin
+49 30 838 51834
immunologie@vetmed.fu-berlin.de

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.