The Role of Innate and Adaptive Immunity in Parkinson's Disease
Open accessAbstract
In recent years, inflammation has become implicated as a major pathogenic factor in the onset and progression of Parkinson's disease. Understanding the precise role for inflammation in PD will likely lead to understanding of how sporadic disease arises. In vivo evidence for inflammation in PD includes microglial activation, increased expression of inflammatory genes in the periphery and in the central nervous system (CNS), infiltration of peripheral immune cells into the CNS, and altered composition and phenotype of peripheral immune cells. These findings are recapitulated in various animal models of PD and are reviewed herein. Furthermore, we examine the potential relevance of PD-linked genetic mutations to altered immune function and the extent to which environmental exposures that recapitulate these phenotypes, which may lead to sporadic PD through similar mechanisms. Given the implications of immune system involvement on disease progression, we conclude by reviewing the evidence supporting the potential efficacy of immunomodulatory therapies in PD prevention or treatment. There is a clear need for additional research to clarify the role of immunity and inflammation in this chronic, neurodegenerative disease.
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Recent studies have indicated that leukocyte infiltration and aberrant inflammation exert protective or detrimental effects on the development of neurodegenerative diseases.
“Recent studies have indicated that leukocyte infiltration and aberrant inflammation exert protective or detrimental effects on the development of neurodegenerative diseases182,183.”
From The WAVE complex in developmental and adulthood brain disorders (2025) · cites this paper as [183]
The “Adaptive Immunity (I): T Lymphocytes in PD” section reports that different T-cell responses worsened or attenuated neurodegeneration in mouse models of Parkinson’s disease. This supports the claim’s protective-or-detrimental distinction, but the paper does not establish it across neurodegenerative diseases generally; its protective example involves regulatory T cells, not aberrant inflammation. (LLM, conf=0.82)
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- Authors
- Kannarkat, G. T., Boss, J. M., & Tansey, M. G.
- Affiliations
- Emory University (US)
- Venue
- Journal of Parkinson’s Disease
- Publisher
- SAGE Publications
- Published
- 2013-01-01
- Volume
- 3
- Issue
- 4
- Pages
- 493-514
- ISSN
- 1877-7171 (ISSN-L)
- 1877-718X
- PMC
- PMC4102262
- OpenAlex
- W1540142856
- Cited by
- 324
- References
- 18
- Citations by year
- 2026: 13 · 2025: 22 · 2024: 33 · 2023: 27 · 2022: 30 · 2021: 37 · 2020: 34 · 2019: 23 · 2018: 30 · 2017: 22 · 2016: 28 · 2015: 16 · 2014: 9
- FWCI
- 2.28
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Parkinson s Disease (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Michael J. Fox Foundation for Parkinson's Research
- National Institutes of Health
- National Institute of General Medical Sciences (T32GM008169, R01GM047310, R01 GM47310-16)
- National Institute of Neurological Disorders and Stroke (F31NS081830, R01NS072467)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- Parkinson's disease, neuroinflammation, innate immunity, adaptive immunity, microglial activation, peripheral immune cells, environmental risk factors, immunomodulatory therapy, neurodegeneration
- MeSH terms
- Animals, Antibodies, B-Lymphocytes, Central Nervous System, Immunity, Innate, Major Histocompatibility Complex, Mutation, Parkinson Disease, T-Lymphocytes, Microglia, Adaptive Immunity, Immunomodulation
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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