Microglial PD-1 stimulation by astrocytic PD-L1 suppresses neuroinflammation and Alzheimer’s disease pathology
Open accessAbstract
Chronic neuroinflammation is a pathogenic component of Alzheimer’s disease (AD) that may limit the ability of the brain to clear amyloid deposits and cellular debris. Tight control of the immune system is therefore key to sustain the ability of the brain to repair itself during homeostasis and disease. The immune‐cell checkpoint receptor/ligand pair PD‐1/PD‐L1, known for their inhibitory immune function, is expressed also in the brain. Here, we report upregulated expression of PD‐L1 and PD‐1 in astrocytes and microglia, respectively, surrounding amyloid plaques in AD patients and in the APP/PS1 AD mouse model. We observed juxtamembrane shedding of PD‐L1 from astrocytes, which may mediate ectodomain signaling to PD‐1‐expressing microglia. Deletion of microglial PD‐1 evoked an inflammatory response and compromised amyloid‐β peptide (Aβ) uptake. APP/PS1 mice deficient for PD‐1 exhibited increased deposition of Aβ, reduced microglial Aβ uptake, and decreased expression of the Aβ receptor CD36 on microglia. Therefore, ineffective immune regulation by the PD‐1/PD‐L1 axis contributes to Aβ plaque deposition during chronic neuroinflammation in AD. Neuroinflammation, a hallmark of Alzheimer’s disease (AD), is involved in beta‐amyloid peptide (Aβ) plaque deposition and clearance. Here, the PD‐1/PD‐L1 axis is found as an important pathway for regulating the immune system in the brain, sustaining microglial Aβ uptake and reducing chronic neuroinflammation. The immune‐checkpoint receptor/ligand pair PD‐1/PD‐L1 sustains phagocytic function of microglia to prevent Aβ plaque deposition in APP/PS mouse models and patient tissues.
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A majority of Alzheimer's disease risk genes identified through genome-wide association studies are highly expressed in microglia, suggesting a key role in microglial dysfunction.
“A majority of AD risk genes identified through genome-wide association studies are highly expressed in microglia, the brain’s innate immune cells, suggesting a key role in microglial dysfunction (Kummer et al., 2021; Penney et al., 2020; Teipel et al., 2022).”
From A novel molecular class that recruits HDAC/MECP2 complexes to PU.1 motifs reduces neuroinflammation (2023) · cites this paper as Kummer et al., 2021
The Results section ('PD-1 regulates microglial Aβ uptake and inflammation'; page unavailable) links altered microglial gene expression to inflammatory pathways, supporting a role for microglial dysfunction in AD pathology. It does not say that a majority of GWAS-identified AD risk genes are highly expressed in microglia; searches for 'genome-wide association studies' and 'GWAS risk genes' found no such passage. (LLM, conf=0.82)
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- Authors
- Kummer, M. P., Ising, C., Kummer, C., Sarlus, H., Griep, A., Vieira‐Saecker, A., Schwartz, S., Halle, A., Brückner, M., Händler, K., Schultze, J. L., Beyer, M., Latz, E., & Heneka, M. T.
- Affiliations
- University of Bonn (DE)
- German Center for Neurodegenerative Diseases (DE)
- Center of Advanced European Studies and Research (DE)
- Corresponding author
- Kummer, Markus P
- Heneka, Michael T
- ORCID
- Venue
- The EMBO Journal
- Published
- 2021-11-26
- Volume
- 40
- Issue
- 24
- Pages
- e108662-e108662
- ISSN
- 0261-4189 (ISSN-L)
- 1460-2075
- PMC
- PMC8672180
- OpenAlex
- W3215791278
- Cited by
- 127
- References
- 55
- Citations by year
- 2026: 22 · 2025: 28 · 2024: 42 · 2023: 24 · 2022: 10 · 2021: 1
- FWCI
- 9.38
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- The EMBO Journal (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Open Repository and Bibliography (University of Luxembourg) (submittedVersion, other-oa)
- DZNE Pub (submittedVersion, other-oa)
- Funders
- European Union Seventh Framework Program (INMIND)
- Deutsche Forschungsgemeinschaft (KFO177, IS 299/3‐1, EXC2151‐390873048)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Keywords
- Alzheimer's disease, neuroinflammation, PD-1/PD-L1 axis, microglia, astrocytes, amyloid plaques, amyloid-beta uptake, CD36, APP/PS1 mice, immune checkpoint, phagocytosis, amyloid-beta clearance, ectodomain shedding
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Animals, Astrocytes, Disease Models, Animal, Female, HeLa Cells, Humans, Male, Mice, Transgenic, Middle Aged, Up-Regulation, Case-Control Studies, Amyloid beta-Protein Precursor, Gene Deletion, Microglia, CD36 Antigens, Mice, HEK293 Cells, B7-H1 Antigen, Programmed Cell Death 1 Receptor
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