| First Author | Xiao W | Year | 2019 |
| Journal | J Neuroimmunol | Volume | 333 |
| Pages | 576970 | PubMed ID | 31146104 |
| Mgi Jnum | J:289423 | Mgi Id | MGI:6435043 |
| Doi | 10.1016/j.jneuroim.2019.576970 | Citation | Xiao W, et al. (2019) The role of Interleukin-33 in the modulation of splenic T-cell immune responses after experimental ischemic stroke. J Neuroimmunol 333:576970 |
| abstractText | 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 30min of middle cerebral artery occlusion (MCAO) for ischemic stroke induction. Recombinant mouse IL-33 (100mug/kg) was pre-treated intraperitoneally at 30min 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-gamma(+) T cells and increased Foxp3(+) T cells in the spleen tissues. Meanwhile, IL-33 pre-treatment could decrease the production of IFN-gamma and increase the secretion of IL-4, IL-10 and TGF-beta from the spleen at 24h 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. |
