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- W4253092337 abstract "Abstract Increasing evidences reveal that the peripheral immune system is involved in the pathogenesis of Alzheimer's disease (AD). Here, we report that pulmonary B lymphocytes mitigate beta-Amyloid (Aβ) pathology in 5xFAD mice. The proportion of B cells, rather than T cells, increases within the brain, meningeal and lung tissues in 3-month-old 5xFAD mice. Deletion of mature B cells aggravates Aβ load and memory deficits of 5xFAD mice. Mechanistically, pulmonary B cells can migrate to the brain parenchyma and produce interleukin-35, which inhibits neuronal β-site APP-cleaving enzyme 1 expression, and subsequently reduces the production of Aβ. In turn, pulmonary B cell proliferation is associated with activation of the toll-like receptor/nuclear factor kappa-B pathway through elevated Aβ that is drained from the brain parenchyma to the lungs via meningeal lymphatics. Furthermore, promoting pulmonary B cell proliferation via overexpression of B-cell-activating factor ameliorates brain Aβ load and improves cognitive functions of 10-month-old 5xFAD mice. Together, these results highlight the lungs as both immune targets and effector organs in Aβ pathogenesis. Pulmonary B cells could serve as a potential target against AD." @default.
- W4253092337 created "2022-05-12" @default.
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- W4253092337 date "2021-07-19" @default.
- W4253092337 modified "2023-10-16" @default.
- W4253092337 title "Pulmonary B Lymphocytes Ameliorate Alzheimer's Disease-Like Neuropathology" @default.
- W4253092337 doi "https://doi.org/10.21203/rs.3.rs-713746/v1" @default.
- W4253092337 hasPublicationYear "2021" @default.
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