Excerpt: "... To investigate the impact of CCL5 on early-stage amyloid pathology in vivo, we intracerebroventricularly injected CCL5 into AppNL-G-F; Cd3e–/– mice at 6–7 weeks of age, resulting in increased Aβ plaque deposition after 6–7 weeks (Fig. 5g). Conversely, anti-CCL5 antibody into AppNL-G-F mouse brains at 6 and 10 weeks of age reduced Aβ plaque deposition, with a trend towards increased CD11c+ plaque-associated microglia 4 weeks after the final injection (Fig. 5h, i). These in vivo results indicate that microglia express high levels of CCR5 in response to amyloid pathology, and its ligand CCL5, produced by brain CD8+ T cells, suppresses microglial transition to disease-associated states. This suppression leads to increased Aβ plaque deposition during the early stages of amyloid pathology.

https://www.nature.com/articles/s41467-025-64503-x