Interleukin-6, a mental cytokine

Spooren, Anneleen; Kolmus, Krzysztof; Laureys, Guy; Clinckers, Ralph; De Keyser, Jacques; Haegeman, Guy; Gerlo, Sarah

doi:10.1016/j.brainresrev.2011.01.002

Cited by 352Neuroinflammation and Neurodegeneration MechanismsCytokine Signaling Pathways and InteractionsTryptophan and brain disorders

Interleukin-6, a mental cytokine

Spooren, Anneleen, Kolmus, Krzysztof, Laureys, Guy, Clinckers, Ralph, De Keyser, Jacques, Haegeman, Guy, Gerlo, Sarah·2011·Brain Research Reviews

DOI 10.1016/j.brainresrev.2011.01.002

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Abstract

Almost a quarter of a century ago, interleukin-6 (IL-6) was discovered as an inflammatory cytokine involved in B cell differentiation. Today, IL-6 is recognized to be a highly versatile cytokine, with pleiotropic actions not only in immune cells, but also in other cell types, such as cells of the central nervous system (CNS). The first evidence implicating IL-6 in brain-related processes originated from its dysregulated expression in several neurological disorders such as multiple sclerosis, Alzheimer's disease and Parkinson's disease. In addition, IL-6 was shown to be involved in multiple physiological CNS processes such as neuron homeostasis, astrogliogenesis and neuronal differentiation. The molecular mechanisms underlying IL-6 functions in the brain have only recently started to emerge. In this review, an overview of the latest discoveries concerning the actions of IL-6 in the nervous system is provided. The central position of IL-6 in the neuroinflammatory reaction pattern, and more specifically, the role of IL-6 in specific neurodegenerative processes, which accompany Alzheimer's disease, multiple sclerosis and excitotoxicity, are discussed. It is evident that IL-6 has a dichotomic action in the CNS, displaying neurotrophic properties on the one hand, and detrimental actions on the other. This is in agreement with its central role in neuroinflammation, which evolved as a beneficial process, aimed at maintaining tissue homeostasis, but which can become malignant when exaggerated. In this perspective, it is not surprising that 'well-meant' actions of IL-6 are often causing harm instead of leading to recovery.

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In cell culture, Aβ stimulates IL-6 release, which leads to microglial differentiation, thought to further enable them to degrade Aβ.
“In cell culture, Aβ stimulates IL-6 release which leads to microglial differentiation, thought to further enable them to degrade Aβ [154].”
From Glial contributions to neurodegeneration in tauopathies (2017) · cites this paper as [154]
IL-6 can activate JAK-STAT pathways, NMDA receptors, and p38-MAPK kinases, which all have been shown to contribute to p-tau formation.
“IL-6 can also activate JAK-STAT pathways, NMDA receptors, and p38-MAPK kinases which all have been shown to contribute to p-tau formation [154, 159].”
From Glial contributions to neurodegeneration in tauopathies (2017) · cites this paper as [154]

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“Low concentrations of IL-6 (below 5 ng/ml) have no effect in certain systems (Carlson et al., 1999; Peng et al., 2005).”
Background
Interleukin-6 improves the survival of mesencephalic catecholaminergic and septal cholinergic neurons from postnatal, two-week-old rats in cultures
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“It exerts neurotrophic actions and is also a mediator of acute inflammation [70].”
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Authors: Spooren, A., Kolmus, K., Laureys, G., Clinckers, R., De Keyser, J., Haegeman, G., & Gerlo, S.
Affiliations: Ghent University (BE)
Vrije Universiteit Brussel (BE)
Corresponding author: Spooren, Anneleen
ORCID: Kolmus, Krzysztof
Laureys, Guy
Gerlo, Sarah
Venue: Brain Research Reviews
Publisher: Elsevier BV
Published: 2011-06
Volume: 67
Issue: 1-2
Pages: 157-183
ISSN: 0165-0173 (ISSN-L)
DOI: 10.1016/j.brainresrev.2011.01.002
OpenAlex: W2030593831
Cited by: 352
References: 325
Citations by year: 2026: 6 · 2025: 10 · 2024: 25 · 2023: 20 · 2022: 21 · 2021: 20 · 2020: 22 · 2019: 25 · 2018: 19 · 2017: 30 · 2016: 22 · 2015: 29 · 2014: 34 · 2013: 30 · 2012: 26
FWCI: 2.89
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: Brain Research Reviews (publishedVersion)
PubMed (publishedVersion)
Ghent University Academic Bibliography (Ghent University) (publishedVersion)
Ghent University Academic Bibliography (Ghent University) (submittedVersion)
VUBIR (Vrije Universiteit Brussel) (submittedVersion)
Funders: Fonds Wetenschappelijk Onderzoek
Vlaamse regering
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Keywords: interleukin-6, neuroinflammation, neurodegeneration, Alzheimer's disease, multiple sclerosis, Parkinson's disease, excitotoxicity, neurotrophic effects, astrogliogenesis, neuronal differentiation, central nervous system, cytokines
MeSH terms: Animals, Mental Disorders, Brain Damage, Chronic, Humans, Inflammation, Interleukin-6, Cell Death, Neurodegenerative Diseases

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Interleukin-6, a mental cytokine

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