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34 reviewsMatteo Calgaro 5, Nicola Vitulo 5, Monica Castellucci3, Daniela Cecconi 2,5,1234567890():,;1234567890():,;Check for updatesJessica Brandi 5, Nikolaos Vareltzakis 1, Fabiana Mainieri1, Antonella Calore 1,Gabriele Angelini1, Bruno Bonetti6 & Gabriela Constantin 1,2Immune mechanisms contribute to the neuropathology of Alzheimer’s disease(AD) but the role of adaptive immune cells is unclear. Here we show that thebrain CD8+ T cell compartment is dysregulated in AD patients and in the 3xTgAD mouse model, accumulating activated CD103– tissue-resident memory Tcells that produce large amounts of granzyme K (GrK). These CD103–CD8+T cells originate from the circulation and migrate into the brain using LFA-1integrin. Ablation of brain CD103–CD8+ T cells in 3xTg-AD mice amelioratescognitive decline and reduces neuropathology. GrK induces neuronal dysfunction and tau hyperphosphorylation in human and mouse cells viaprotease-activated receptor-1 (PAR-1), which is expressed at higher levels in theAD brain, revealing a key immune-mediated neurotoxic axis. We conclude thatcommunication between CD8+ T cells and the nervous system is altered in AD,paving the way for therapies targeting T cell-dependent neurotoxicinflammation.
