Cited by 324Parkinson's Disease Mechanisms and TreatmentsNeuroinflammation and Neurodegeneration MechanismsNuclear Receptors and Signaling

The Role of Innate and Adaptive Immunity in Parkinson's Disease

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Kannarkat, George T., Boss, Jeremy M., Tansey, Malú G.·2013·Journal of Parkinson’s Disease

Abstract

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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Cited by

Sorted by citations

Authors
Kannarkat, G. T., Boss, J. M., & Tansey, M. G.
Affiliations
Emory University (US)
Venue
Journal of Parkinson’s Disease
Published
2013-01-01
Volume
3
Issue
4
Pages
493-514
ISSN
  • 1877-7171 (ISSN-L)
  • 1877-718X
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
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

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