Type‐1 interferons contribute to the neuroinflammatory response and disease progression of the MPTP mouse model of Parkinson's disease

Main, Bevan S.; Zhang, Moses; Brody, Kate M.; Ayton, Scott; Frugier, Tony; Steer, David; Finkelstein, David; Crack, Peter J.; Taylor, Juliet M.

doi:10.1002/glia.23028

Cited by 100Parkinson's Disease Mechanisms and TreatmentsNeuroinflammation and Neurodegeneration Mechanismsinterferon and immune responses

Type‐1 interferons contribute to the neuroinflammatory response and disease progression of the MPTP mouse model of Parkinson's disease

Main, Bevan S., Zhang, Moses, Brody, Kate M., Ayton, Scott, Frugier, Tony, Steer, David, Finkelstein, David, Crack, Peter J. +1 more·2016·Glia

DOI 10.1002/glia.23028

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Abstract

Type‐1 interferons (IFNs) are pleiotropic cytokines with a critical role in the initiation and regulation of the pro‐inflammatory response. However, the contribution of the type‐1 IFNs to CNS disorders, specifically chronic neuropathologies such as Parkinson's disease is still unknown. Here, we report increased type‐1 IFN signaling in both post mortem human Parkinson's disease samples and in the 1‐methyl‐4‐phenyl‐1, 2, 3, 6‐tetrahydropyridine (MPTP) mouse model. In response to MPTP, mice lacking the type‐1 IFN receptor (IFNAR1−/−) displayed decreased type‐1 IFN signaling, an attenuated pro‐inflammatory response and reduced loss of dopaminergic neurons. The neuroprotective potential of targeting the type‐1 IFN pathway was confirmed by reduced neuroinflammation and DA cell death in mice treated with a blocking monoclonal IFNAR1 (MAR‐1) antibody. The MPTP/MAR‐1 treated mice also displayed increased striatal dopamine levels and improved behavioural outcomes compared to their MPTP/IgG controls. These data, implicate for the first time, a deleterious role for the type‐1 IFNs as key modulators of the early neuroinflammatory response and therefore the neuronal cell death in Parkinson's disease. GLIA 2016;64:1590–1604

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Absence of endocytosed TLR4 may avoid excessive inflammation and neurotoxicity.
“The absence of endocytosed TLR4 may prevent Ifnb1 induction or increase of p-IFR3 (S396) level, despite the activation of NF-κB signaling, thus avoiding excessive inflammation and neurotoxicity59.”
From Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration (2020) · cites this paper as [59]
Absence of endocytosed TLR4 may prevent increase of p-IFR3 (S396) level.
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From Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration (2020) · cites this paper as [59]
In humans, Parkinson's disease is associated with neuroinflammation in both postmortem and in vivo analyses.
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From Brain-Derived Neurotrophic Factor in Brain Disorders: Focus on Neuroinflammation (2019) · cites this paper as [171]

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Adverse Outcome Pathway on Inhibition of the mitochondrial complex I of nigro-striatal neurons leading to parkinsonian motor deficits
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STING-Mediated Autophagy Is Protective against H2O2-Induced Cell Death
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Regulation of IFN-Is by MEF2D Promotes Inflammatory Homeostasis in Microglia
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STING-triggered CNS inflammation in human neurodegenerative diseasesPreprint
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The cGAS-STING pathway in aging and neurological diseases: From mechanisms to treatment
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Additional file 1 of MicroRNA-218-5p-Ddx41 axis restrains microglia-mediated neuroinflammation through downregulating type I interferon response in a mouse model of Parkinson’s disease
Wang, D., Hongling, G., Qin, Q., Li, J., Zhao, J., Qu, Y., Li, J., 熊永洁, Min, Z., Mao, Z., et al. (2024) · Figshare · doi:10.6084/m9.figshare.25010473
Additional file 1 of Single cell analysis reveals the roles and regulatory mechanisms of type-I interferons in Parkinson’s disease
Quan, P., Li, X., Si, Y., Sun, L., Ding, F. F., Fan, Y., Liu, H., Wei, C., Li, R., Zhao, X., et al. (2024) · Figshare · doi:10.6084/m9.figshare.25530327
Additional file 6 of Prodromal Parkinson disease signs are predicted by a whole-blood inflammatory transcriptional signature in young Pink1−/− rats
Lechner, S., Barnett, D. G. S., Gammie, S. C., & Kelm‐Nelson, C. A. (2024) · Figshare · doi:10.6084/m9.figshare.26688419
Additional file 1 of Prodromal Parkinson disease signs are predicted by a whole-blood inflammatory transcriptional signature in young Pink1−/− rats
Lechner, S., Barnett, D. G. S., Gammie, S. C., & Kelm‐Nelson, C. A. (2024) · Figshare · doi:10.6084/m9.figshare.26688404
Additional file 3 of Single cell analysis reveals the roles and regulatory mechanisms of type-I interferons in Parkinson’s disease
Quan, P., Li, X., Si, Y., Sun, L., Ding, F. F., Fan, Y., Liu, H., Wei, C., Li, R., Zhao, X. L., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26701096
Additional file 3 of Prodromal Parkinson disease signs are predicted by a whole-blood inflammatory transcriptional signature in young Pink1−/− rats
Lechner, S., Barnett, D. G. S., Gammie, S. C., & Kelm‐Nelson, C. A. (2024) · Figshare · doi:10.6084/m9.figshare.26688410
Additional file 5 of Prodromal Parkinson disease signs are predicted by a whole-blood inflammatory transcriptional signature in young Pink1−/− rats
Lechner, S., Barnett, D. G. S., Gammie, S. C., & Kelm‐Nelson, C. A. (2024) · Figshare · doi:10.6084/m9.figshare.26688416
Additional file 2 of Prodromal Parkinson disease signs are predicted by a whole-blood inflammatory transcriptional signature in young Pink1−/− rats
Lechner, S., Barnett, D. G. S., Gammie, S. C., & Kelm‐Nelson, C. A. (2024) · Figshare · doi:10.6084/m9.figshare.26688407
Additional file 2 of Single cell analysis reveals the roles and regulatory mechanisms of type-I interferons in Parkinson’s disease
Quan, P., Li, X., Si, Y., Sun, L., Ding, F. F., Fan, Y., Liu, H., Wei, C., Li, R., Zhao, X., et al. (2024) · Figshare · doi:10.6084/m9.figshare.25530423
Additional file 4 of Prodromal Parkinson disease signs are predicted by a whole-blood inflammatory transcriptional signature in young Pink1−/− rats
Lechner, S., Barnett, D. G. S., Gammie, S. C., & Kelm‐Nelson, C. A. (2024) · Figshare · doi:10.6084/m9.figshare.26688413
Type I Interferons Drive the Gastrointestinal Inflammatory Response in a Mouse Model of Parkinson’s Disease
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Interferon-β Deficiency Selectively Modulates Chronic Microglial Pathways after Traumatic Brain Injury
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ISGylation of STING contributes to neuroinflammation and neurodegeneration via activating c-Fos in Parkinson's disease modelsPreprint
Liu, X. Y., Xu, S., Huang, P., Jiang, X., Dong, A., Wu, T., Huang, T., Ye, Q., & Huang, E. (2026) · Research Square · doi:10.21203/rs.3.rs-10118411/v1
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The contribution of type-I IFN-mediated neuroinflammation to Parkinson's disease progression
Chen, S., Crack, P. J., & Taylor, J. M. (2025) · Brain Behavior & Immunity - Health · doi:10.1016/j.bbih.2025.101017 · Cited by 6 · see citing works
Self-citation
Type-I interferon signaling is pro-inflammatory in models of Parkinson's disease
Main, B. S., Zhang, M., Ayton, S., Finkelstein, D., Crack, P. J., & Taylor, J. M. (2012) · Journal of Neuroimmunology
Self-citation
Type-I interferons in Parkinson's disease: innate inflammatory response drives fate of neurons in model of degenerative brain disorder: An editorial comment on 'Type-I interferons mediate the neuroinflammatory response and neurotoxicity induced by rotenone'
Kanninen, K. M., & White, A. R. (2017) · UEF eRepo (University of Eastern Finland)
The neuroinflammatory response induced by MPTP is altered in mice lacking the type-I interferon-alpha receptor-1 (IFNAR1)
Taylor, J., Main, B. D., Zhang, M. Y., Ayton, S., Finkelstein, D., & Crack, P. J. (2013) · Movement Disorders
Self-citation
Type‐I interferons in Parkinson's disease: innate inflammatory response drives fate of neurons in model of degenerative brain disorder
Kanninen, K. M., & White, A. R. (2017) · Journal of Neurochemistry · doi:10.1111/jnc.13983 · Cited by 4 · see citing works

Authors: Main, B. S., Zhang, M., Brody, K. M., Ayton, S., Frugier, T., Steer, D., Finkelstein, D., Crack, P. J., & Taylor, J. M.
Affiliations: The University of Melbourne (AU)
Florey Institute of Neuroscience and Mental Health (AU)
Monash University (AU)
Corresponding author: Taylor, Juliet M.
ORCID: Main, Bevan S.
Brody, Kate M.
Ayton, Scott
Frugier, Tony
Steer, David
Finkelstein, David
Crack, Peter J.
Taylor, Juliet M.
Venue: Glia
Publisher: Wiley
Published: 2016-07-12
Volume: 64
Issue: 9
Pages: 1590-1604
ISSN: 0894-1491 (ISSN-L)
1098-1136
DOI: 10.1002/glia.23028
OpenAlex: W2476939147
Cited by: 92
References: 57
Citations by year: 2026: 5 · 2025: 11 · 2024: 13 · 2023: 16 · 2022: 7 · 2021: 6 · 2020: 6 · 2019: 11 · 2018: 10 · 2017: 6 · 2016: 1
FWCI: 7.02
Type: journal article
Language: en
Open access: closed
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Glia (publishedVersion)
PubMed (publishedVersion)
Minerva Access (University of Melbourne) (submittedVersion)
Funders: University of Melbourne Early Career Fellowship (JMT) and Rotary Australia Postgraduate Scholarship (BSM)
Topics: Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
Keywords: type I interferon, Parkinson's disease, neuroinflammation, MPTP mouse model, IFNAR1, dopaminergic neuron death, neuroprotection, striatal dopamine, disease progression
MeSH terms: Animals, Disease Models, Animal, Dopamine, Inflammation, Interferon Type I, Mice, Inbred C57BL, Parkinson Disease, Substantia Nigra, Cytokines, Cell Death, Microglia, Mice, Knockout, Dopaminergic Neurons

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Type‐1 interferons contribute to the neuroinflammatory response and disease progression of the MPTP mouse model of Parkinson's disease

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