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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]