Regulatory T cells modulate inflammation and reduce infarct volume in experimental brain ischaemia

David Brea, Jesús Agulla, Manuel Rodríguez-Yáñez, David Barral, Pedro Ramos-Cabrer, Francisco Campos, Angeles Almeida, Antoni Dávalos, José Castillo

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56 Citations (Scopus)


© 2014 The Authors. Brain ischaemia (stroke) triggers an intense inflammatory response predominately mediated by the accumulation of inflammatory cells and mediators in the ischaemic brain. In this context, regulatory T (Treg) cells, a subpopulation of CD4+ T cells with immunosuppressive and antiinflammatory properties, are activated in the late stages of the disease. To date, the potential therapeutic usefulness of Treg cells has not been tested. In this study, we aimed to investigate whether Treg cells exert protection/repair following stroke. Both the adoptive transfer of Treg cells into ischaemic rats and the stimulation of endogenous T-cell proliferation using a CD28 superagonist reduced the infarct size at 3-28 days following the ischaemic insult. Moreover, T cell-treated animals had higher levels of FoxP3 and lower levels of IL-1β, CD11b+ and CD68+ cells in the infarcted hemisphere when compared with control animals. However, T-cell treatment did not alter the rate of proliferation of NeuN-, NCAMor CD31-positive cells, thereby ruling out neurogenesis and angiogenesis in protection. These results suggest that adoptive transfer of T cells is a promising therapeutic strategy against the neurological consequences of stroke.
Original languageEnglish
Pages (from-to)1571-1579
JournalJournal of Cellular and Molecular Medicine
Issue number8
Publication statusPublished - 1 Jan 2014


  • Cerebrovascular disease/stroke
  • Immunomodulation
  • Inflammation
  • Regulatory T cells


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