TNF-alpha expression by resident microglia and infiltrating leukocytes in the central nervous system of mice with experimental allergic encephalomyelitis. Regulation by Th1 cytokines.

Renno, T; Krakowski, M; Piccirillo, C; Lin, J Y; Owens, T

doi:10.4049/jimmunol.154.2.944

Cited by 401Multiple Sclerosis Research StudiesNeuroinflammation and Neurodegeneration MechanismsT-cell and B-cell Immunology

TNF-alpha expression by resident microglia and infiltrating leukocytes in the central nervous system of mice with experimental allergic encephalomyelitis. Regulation by Th1 cytokines.

Renno, T, Krakowski, M, Piccirillo, C, Lin, J Y, Owens, T·1995·The Journal of Immunology

DOI 10.4049/jimmunol.154.2.944

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Abstract

The inflammatory cytokines IFN-gamma and TNF-alpha have been demonstrated in various autoimmune diseases, and are thought to participate in the induction and pathogenesis of disease. TFN-alpha is a cytopathic cytokine that is cytotoxic for oligodendrocytes in vitro and has been implicated in the pathology of multiple sclerosis and its animal model experimental allergic encephalomyelitis (EAE). We used reverse transcriptase (RT)-PCR to study the kinetics, cellular source, and regulation of cytokine gene expression in the central nervous system (CNS) of SJL/J mice with myelin basic protein-induced EAE at different stages of the disease. The expression of CD3, IL-2, IFN-gamma, and TNF-alpha mRNA was barely detectable in the CNS of unmanipulated mice or mice that were immunized with adjuvant but showed no symptoms. These mRNAs were readily detectable in the CNS of mice during peak disease, then coordinately dropped to background levels during remission. Analysis of cells isolated from the CNS of mice with acute EAE showed that the Th1 cytokines, IL-2 and IFN-gamma, were produced by infiltrating CD4++ T cells. In contrast, TNF-alpha was predominantly transcribed by non-T mononuclear CNS cells, the majority of which were identified as microglia and macrophages by their Mac-1 phenotype. Microglia could be discriminated by their low expression of CD4+5. Incubation of freshly derived, adult microglia from normal, uninfiltrated, CNS with activated Th1 supernatant induced the production of TNF-alpha mRNA. Therefore, TNF-alpha is made by both CNS-resident microglia and infiltrating macrophages during EAE, and this production is tightly controlled by cytokines secreted by infiltrating CD4++ T cells.

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Upon stimulation by factors such as TLR ligands, Aβ aggregates, complement factors, or opioids, microglia can shift from a homeostatic state to an activated state.
“Upon stimulation by factors such as toll-like receptor (TLR) ligands, β-amyloid (Aβ) aggregates, complement factors, or opioids, microglia can shift from homeostatic state to an activated state.”
From Tubular human brain organoids to model microglia-mediated neuroinflammation (2021) · cites this paper as [4]
Activated microglia can secrete pro-inflammatory cytokines (e.g., TNF-α, IL-6, IL-1β, IL-18) or anti-inflammatory cytokines (e.g., IL-4, IL-10, TGF-β) depending on the dose, frequency, and context of stimulation.
“Activated microglia can either secrete pro-inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, and IL-18 or anti-inflammatory cytokines such as IL-4, IL-10, and transforming growth factor (TGF)-β depending on the dose, frequency, and context of the stimulation.4–7”
From Tubular human brain organoids to model microglia-mediated neuroinflammation (2021) · cites this paper as [4]

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Authors: Renno, T., Krakowski, M., Piccirillo, C., Lin, J. Y., & Owens, T.
Affiliations: Montreal Neurological Institute and Hospital (CA)
ORCID: Renno, T
Piccirillo, C
Lin, J Y
Owens, T
Venue: The Journal of Immunology
Publisher: Oxford University Press (OUP)
Published: 1995-01
Volume: 154
Issue: 2
Pages: 944-953
ISSN: 0022-1767 (ISSN-L)
1550-6606
DOI: 10.4049/jimmunol.154.2.944
OpenAlex: W1512112524
Cited by: 401
References: 0
Citations by year: 2026: 2 · 2025: 1 · 2024: 2 · 2023: 3 · 2022: 6 · 2021: 7 · 2020: 6 · 2019: 6 · 2018: 3 · 2017: 9 · 2016: 10 · 2015: 12 · 2014: 10 · 2013: 9 · 2012: 11
FWCI: 23.59
Type: journal article
Language: en
Open access: closed
Licence: academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations: The Journal of Immunology (publishedVersion)
PubMed (publishedVersion)
University of Southern Denmark Research Portal (University of Southern Denmark) (publishedVersion)
Topics: Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords: TNF-α, experimental autoimmune encephalomyelitis, microglia, macrophages, Th1 cytokines, interferon-gamma, interleukin-2, CD4+ T cells, myelin basic protein, multiple sclerosis, cytokine gene expression, Mac-1, CD45, neuroinflammation, SJL/J mice
MeSH terms: Animals, Base Sequence, Central Nervous System, Encephalomyelitis, Autoimmune, Experimental, Female, Flow Cytometry, Interferon-gamma, Interleukin-2, Leukocytes, Mononuclear, Macrophages, Mice, Inbred Strains, Molecular Sequence Data, RNA, Messenger, Tumor Necrosis Factor-alpha, Polymerase Chain Reaction, Cytokines, CD3 Complex, Microglia, Th1 Cells, Mice

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TNF-alpha expression by resident microglia and infiltrating leukocytes in the central nervous system of mice with experimental allergic encephalomyelitis. Regulation by Th1 cytokines.

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