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IFN-γ Promotes Complement Expression and Attenuates Amyloid Plaque Deposition in Amyloid β Precursor Protein Transgenic Mice
Open accessAbstract
Reactive gliosis surrounding amyloid β (Aβ) plaques is an early feature of Alzheimer’s disease pathogenesis and has been postulated to represent activation of the innate immune system in an apparently ineffective attempt to clear or neutralize Aβ aggregates. To evaluate the role of IFN-γ–mediated neuroinflammation on the evolution of Aβ pathology in transgenic (Tg) mice, we have expressed murine IFN-γ (mIFN-γ) in the brains of Aβ precursor protein (APP) Tg mice using recombinant adeno-associated virus serotype 1. Expression of mIFN-γ in brains of APP TgCRND8 mice results in robust noncell autonomous activation of microglia and astrocytes, and a concomitant significant suppression of Aβ deposition. In these mice, mIFN-γ expression upregulated multiple glial activation markers, early components of the complement cascade as well as led to infiltration of Ly-6c positive peripheral monocytes but no significant effects on APP levels, APP processing or steady-state Aβ levels were noticed in vivo. Taken together, these results suggest that mIFN-γ expression in the brain suppresses Aβ accumulation through synergistic effects of activated glia and components of the innate immune system that enhance Aβ aggregate phagocytosis.
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“Indeed, manipulation of expression of Trem2, Tyrobp, Cx3cl1/Cx3cr1, IL1β, and IFN-γ have all been shown to have opposing effects on amyloid and tau pathologies [49–51, 55–65].”
From Deletion of Abi3/Gngt2 influences age-progressive amyloid β and tau pathologies in distinctive ways (2022) · cites this paper as [60]
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“For amyloid pathology, there is data that activated micro/astroglia enhances Aβ phagocytosis [60, 62, 71]”
From Deletion of Abi3/Gngt2 influences age-progressive amyloid β and tau pathologies in distinctive ways (2022) · cites this paper as [60]
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“administration or expression of IFN-γ, TNF or IL-6 in the mouse CNS reduced Aβ deposition [48–50]”
From Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function (2022) · cites this paper as [48]
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“For example, increased gliosis induced by brain infusion of lipopolysaccharide (4) or overexpression of the inflammatory cytokine interleukin-6 (5) or interferon-γ (6) markedly reduces amyloid plaque burden.”
From Attenuating astrocyte activation accelerates plaque pathogenesis in APP/PS1 mice (2013) · cites this paper as [6]
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“mice overexpressing IL-6 (127) or IFN-γ (128) had enhanced microglial phagocytosis of Aβ accompanied by an increase in complement component mRNA levels, TNF-α, and other inflammatory mediators.”
From Microglia in Alzheimer's disease (2017) · cites this paper as [128]
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“Several studies have found that activating pro-inflammatory pathways — for example, by overexpressing TNF29, IFNγ30 or IL-631, or by inhibiting anti-inflammatory cytokines such as IL-1032 — reduces plaque deposition, and vice versa33,34.”
From Interplay between innate immunity and Alzheimer disease: APOE and TREM2 in the spotlight (2018) · cites this paper as [30]
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Metadata
- Authors
- Chakrabarty, P., Ceballos-Diaz, C., Beccard, A., Janus, C., Dickson, D., Golde, T. E., & Das, P.
- Affiliations
- Mayo Clinic (US)
- Department of Neuroscience, Mayo Clinic , Jacksonville, FL 32224
- University of Florida (US)
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-05-01
- Volume
- 184
- Issue
- 9
- Pages
- 5333-5343
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- PMC
- PMC3798002
- OpenAlex
- W2157079522
- Cited by
- 206
- References
- 71
- Citations by year
- 2026: 2 · 2025: 11 · 2024: 4 · 2023: 10 · 2022: 25 · 2021: 24 · 2020: 15 · 2019: 17 · 2018: 8 · 2017: 12 · 2016: 11 · 2015: 14 · 2014: 13 · 2013: 13 · 2012: 15
- FWCI
- 8.66
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Mayo Clinic
- American Health Assistance Foundation
- National Institutes of Health
- National Institute on Aging (R01 AG18454, P01AG025531, R01AG018454, R01AG029886, R01AG29886, P01AG25531)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- interferon-gamma, amyloid-beta, amyloid plaques, Alzheimer's disease, APP transgenic mice, complement system, reactive gliosis, microglial activation, astrocyte activation, neuroinflammation, innate immunity, AAV gene delivery, phagocytosis, peripheral blood monocytes, TgCRND8 mice
- MeSH terms
- Dependovirus, Alzheimer Disease, Animals, Astrocytes, Cell Line, Chickens, Complement System Proteins, Disease Models, Animal, Female, Humans, Immunity, Innate, Interferon-gamma, Male, Mice, Inbred C57BL, Mice, Transgenic, Neuroglia, Phagocytosis, Protein Processing, Post-Translational, Down-Regulation, Up-Regulation, Amyloid beta-Protein Precursor, Microglia, Mice, Plaque, Amyloid
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