Table 1 Anti-IL-17 and IL-17R
From: The role of Th17 cells/IL-17A in AD, PD, ALS and the strategic therapy targeting on IL-17A
Disease | Model | Intervention | Result | References |
|---|---|---|---|---|
AD | LPS treated rat | IL‐17Ab | IL-17A Abs improved LPS-induced memory impairment | [64] |
AD | Vivo animal model Inject Aβ1-42 into the ventricle | IL‐17Ab, IgG2A, clone 50104 Control: IgG2A, clone 54447 | Preconditioning with IL-17Ab significantly reduced neurodegenerative changes induced by Aβ 1–42, improved memory function, and inhibited the increase of pro-inflammatory mediators in a dose-dependent manner Administration of IL 17Ab after a β 1–42 injection reduced neurodegenerative memory decline and pro-inflammatory mediators and cytokines levels | [65] |
PD | HiPSC-derived neurons of PD | Anti-IL-17/antiIL-17R/secukinumab+ T lymphocyte Control: + T lymphocyte Blank control group | Anti-IL-17Ab, anti-IL-17R, and secukinumab reduced T lymphocyte-induced neuronal death, with no significant difference in cell death levels compared to neurons cultured without T cells | [66] |
PD | MPTP-treated mice MPP+-treated rats | Anti-IL-17Ab | Injection of anti-IL-17Ab into the lateral ventricle of PD rats can improve the activation and dyskinesia of microglia in BBB-disrupting dopaminergic neurodegeneration | [67] |
PD | MPTP-induced PD mice | Anti-IL-17Ab | Anti-IL-17Ab eliminated th17-induced death of DAergic neurons | [68] |
ALS | iPSC-derived MNs (ALS)+ TH-17(ALS/HCs/MS) | Anti-IL-17Ab and anti-IL-17R | Th17 cells and IL-17A did directly promote MN degeneration. Anti-IL-17Ab and anti-IL-17R therapy reversed all effects of IL-17A | [69] |