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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
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)+
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]