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Table 3. Treg cells regulate AD pathogenesis in experimental models

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]