The splenic T-cell immune response to stroke has been identified as an important role in the progression of brain injury following ischemic stroke. Interleukin (IL)-33 as a novel cytokine of IL-1 family has been found to be protective for ischemic brain injury. Here, we determined the contribution of IL-33 to the T-cell immune responses in the spleen after experimental ischemic stroke. Mice were subjected to 30 min of middle cerebral artery occlusion (MCAO) for ischemic stroke induction. Recombinant mouse IL-33 (100 ìg/kg) was pre-treated intraperitoneally at 30 min prior to MCAO, then the percentages of T cell subsets, related cytokines and transcription factors in the spleen tissues were measured. Intraperitoneal IL-33 pre-treatment may attenuate neurological deficit scores and infarct volumes after MCAO, which was accompanied by reduced IFN-ã+ T cells and increased Foxp3+ T cells in the spleen tissues. Meanwhile, IL-33 pre-treatment could decrease the production of IFN-ã and increase the secretion of IL-4, IL-10 and TGF-â from the spleen at 24 h after MCAO. Additionally, the mRNA level of the transcription factor T-bet was downregulated by IL-33, and the levels of GATA-3 and Foxp3 mRNA were upregulated. These results showed that the long-term protective mechanism of IL-33 in ischemic stroke may be partly associated to its modulation role for splenic T-cell immune responses through inhibiting Th1 response and promoting Treg response, suggesting that IL-33 may be a candidate treatment for human stroke via modulating the peripheral immune system following stroke.
Animals Atrophy