| First Author | Campolo M | Year | 2020 |
| Journal | Int J Mol Sci | Volume | 21 |
| Issue | 24 | PubMed ID | 33317145 |
| Mgi Jnum | J:304336 | Mgi Id | MGI:6514491 |
| Doi | 10.3390/ijms21249384 | Citation | Campolo M, et al. (2020) TLR7/8 in the Pathogenesis of Parkinson's Disease. Int J Mol Sci 21(24):9384 |
| abstractText | Neuroinflammation and autoimmune mechanisms have a key part in the pathogenesis of Parkinson's disease (PD). Therefore, we evaluated the role of Toll-like receptors (TLRs) as a link between inflammation and autoimmunity in PD. An in vivo model of PD was performed by administration of 1-metil 4-fenil 1,2,3,6-tetraidro-piridina (MPTP) at the dose of 20 mg/kg every 2 h for a total administration of 80/kg, both in single Knock Out (KO) mice for TLR7, TLR 8, and TLR9 and in double KO mice for TLR 7/8(-/-). All animals were compared with WT animals used as a control group. All animals were sacrificed after 7 days form the first administration of MPTP. The genetic absence of TLR 7 and 8 modified the PD pathway, increasing the immunoreactivity for TH and DAT compared to PD groups and decreasing microglia and astrocytes activation. Moreover, the deletion of TLR7 and TLR8 significantly reduced T-cell infiltration in the substantia nigra and lymph nodes, suggesting a reduction of T-cell activation. Therefore, our result highlights a possibility that an immunotherapy approach, by using a dual antagonist of TLR 7 and 8, could be considered as a possible target to develop new therapies for Parkinson diseases. |
