Background: Alzheimer’s disease (AD) is a neurodegenerative disorder histopathologically
characterized by the accumulation of amyloid β (Aβ) peptides and inflammation associated with activated
microglia. These features are well investigated in the central nervous system using AD-model
mice; however, peripheral inflammation in these mice has not been investigated well.
Objective: We evaluated the inflammatory responses, especially myeloid dendritic cells (mDCs), in peripheral
lymphoid tissues in AD-model mice to determine their association with Aβ deposition.
Methods: We collected lymphocytes from mesenteric lymphoid nodes (MLNs) and Peyer’s patches
(PPs) of 5×FAD transgenic mice used as an AD model. Lymphocytes were analyzed using a flow cytometer
to characterize mDCs and T cells. Collected lymphocytes were treated with Aβ1-42 ex vivo to
evaluate the inflammatory response.
Results: We observed elevated levels of inflammatory cytokines and chemokines including interleukin
(IL)-12 and macrophage inflammatory protein-1α in mDCs from MLNs and PPs and reduced levels of
programmed death-ligand-1, an immunosuppressive co-stimulatory molecule, on the surface of mDCs
from 5×FAD mice. Additionally, we found increases in interferon (IFN)-γ-producing CD4- or CD8-
positive T cells in MLNs were increased in 5×FAD mice. Moreover, ex vivo treatment with Aβ peptides
increased the production of IL-12 and IFN-γ by lymphocytes from 5×FAD mice.
Conclusion: The present study showed that pro-inflammatory mDC and T cells were induced in MLNs
and PPs of 5×FAD mice.