From: Peripheral immune system in aging and Alzheimer’s disease
Subset | Location | AD model | Specificity | Effects on pathogenesis | Reference |
---|---|---|---|---|---|
Treg | Systemic | APP/PS1 | bulk | Transient depletion of Treg accelerated cognitive decline; increased Treg with low-dose IL-2 treatment restored cognitive functions | [129] |
Treg | Systemic | 3xTg | bulk | Adoptively transferred cells improved cognitive functions and reduced Aβ deposition; long-term Treg depletion resulted in exacerbated spatial learning deficits, Aβ plaque load and microgliosis | [130] |
Treg | Systemic and Parenchyma | App/PS1 ΔE9 | bulk | AAV-IL-2 expression within the brain induced Treg expansion and astrocyte activation, reduced Aβ plaque and improved synaptic plasticity and spine density | [131] |
Treg | Systemic | AβPPswe/PS1 Δ E9 | bulk | Adoptively transferred cells improved cognitive function, while reducing Aβ deposition, microgliosis and systematic inflammation | [132] |
Treg | Systemic | 5xFAD APP/PS1 | bulk | Transient depletion or pharmacological inhibition of Treg lead to Aβ plaque clearance, reduced neuroinflammation and reversal of cognitive decline. It affected CP with increased recruitment of peripheral monocytes and Tregs to Aβ plaque | [125] |
Treg | Systemic | 5xFAD | bulk | Anti-PD1 treatment stimulated IFNƔ-dependent systematic immune response, which resulted in the recruitment of peripheral monocytes and Tregs to Aβ plaque, clearance of plaque, and improvement of cognitive performance. Repeated treatments maintained a long-lasting beneficial effects | [134] |
Treg | ThyAPP/PS1m146L ThyAPP/PS1A246E PD-APP | bulk | Anti-PD1 treatments had no effect on amyloid pathology nor induced infiltration of peripheral monocyte into the brain | [135] |