| First Author | Yu A | Year | 2017 |
| Journal | Int Immunopharmacol | Volume | 53 |
| Pages | 143-148 | PubMed ID | 29107214 |
| Mgi Jnum | J:272784 | Mgi Id | MGI:6282396 |
| Doi | 10.1016/j.intimp.2017.10.023 | Citation | Yu A, et al. (2017) Tim-3 enhances brain inflammation by promoting M1 macrophage polarization following intracerebral hemorrhage in mice. Int Immunopharmacol 53:143-148 |
| abstractText | Macrophage polarization contributes to brain inflammation following spontaneous intracerebral hemorrhage (ICH). T cell immunoglobulin and mucin domain-3 (Tim-3) has been identified to induce macrophage mediated inflammation following ICH. However, the regulation of Tim-3 on macrophage polarization following ICH has not been fully studied. In current experiment, we explored Tim-3 expression, macrophage polarization, brain water content and neurological function in WT and Tim-3(-)/(-) ICH mice. In addition, downstream transcriptional factor TRIF and IRF3 were also analyzed. We found that ICH promoted Tim-3 expression and M1 polarization in the perihematomal region of WT mice, leading to increased brain water content and neurological impairment. However, deletion of Tim-3 expression attenuated M1 polarization, decreased rain water content and improved neurological function of ICH mice. Furthermore, Tim-3 signal promoted transcriptional factors TRIF and IRF3 levels, regulating macrophage polarization. The data suggested that Tim-3 played a crucial role in the macrophage polarization and brain inflammation following ICH, and might represent a promising way in ICH therapy. |
