ArticleActa pharmacologica Sinica2026
Lung memory B cells ameliorate Alzheimer's disease-like pathology in 5×FAD mice through the CXCL12-CXCR4 axis.
Article in Acta pharmacologica Sinica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed.
- Central nervous system lymphatic network: from the maintenance of brain homeostasis to emerging therapeutic perspectives in neurodegenerative diseases.Translational neurodegeneration · 2026Review
- Exploring the lung-brain axis in perioperative neurocognitive disorders: a potential therapeutic target.Molecular psychiatry · 2026Article
- Microglia and neuroinflammation: function, heterogeneity, and crosstalk.Cellular & molecular immunology · 2026Review
- Expanding roles of cGAS-STING signaling in neuroinflammation.The Journal of clinical investigation · 2026Review
- The lung-brain axis: elucidating the mechanisms of pulmonary-driven neurological disorders.Journal of neuroinflammation · 2026Review
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16 authors.
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Abstract
Although most AD-related pathological studies are limited to the brain, increasing evidence has demonstrated the contribution of peripheral immune cells to the pathogenesis of AD. We recently demonstrated that meningeal B cells inhibit β-amyloid (Aβ) production in the frontal cortex of young 5×FAD mice. In this study, we explored the precise origin of meningeal B cells. We observed that the AD-like pathology in 5×FAD mice was exacerbated when the germinal center in the lung lymph nodes was specifically destroyed via the intratracheal instillation of anti-CD40 antibodies, whereas it was alleviated via the intratracheal instillation of AAV-mBAFF to overexpress B-cell activating factor in the lungs. We demonstrated that Aβ was drained from the brain via meningeal lymphatics and eventually traveled to the lungs, where it activated B cells via the TLR4/NF-ĸB signaling pathway, whereas the CXCL12-CXCR4 axis regulated lung B-cell infiltration into the frontal cortex. We revealed that the increased number of B cells in the lungs of 5×FAD mice mainly included memory B (Bmem) cells. The supplementation of lung Bmem cells mitigated AD-like pathology in B-cell-deficient μMT
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