ArticleJournal of neuroinflammation2016
Sustained TNF production by central nervous system infiltrating macrophages promotes progressive autoimmune encephalomyelitis.
Article in Journal of neuroinflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 58 citations in OpenAlex.
- Review
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- PD-L1 positive astrocytes attenuate inflammatory functions of PD-1 positive microglia in models of autoimmune neuroinflammation.Nature communications · 2023Article
- Comparison of recent updates in genetics, immunology, biomarkers, and neuroimaging of primary-progressive and relapsing-remitting multiple sclerosis and the role of ocrelizumab in the management of their refractory cases.Health science reports · 2023Article
- Delimiting MOGAD as a disease entity using translational imaging.Frontiers in neurology · 2023Review
- Specific myeloid signatures in peripheral blood differentiate active and rare clinical phenotypes of multiple sclerosis.Frontiers in immunology · 2023Article
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- Chronic Toxoplasma gondii infection contributes to perineuronal nets impairment in the primary somatosensory cortex.Parasites & vectors · 2022Article
- The therapeutic potential of bone marrow-derived macrophages in neurological diseases.CNS neuroscience & therapeutics · 2022Review
- Intranasal delivery of a small-molecule ErbB inhibitor promotes recovery from acute and late-stage CNS inflammation.JCI insight · 2022Article
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Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundTumor necrosis factor (TNF) has pleiotropic functions during both the demyelinating autoimmune disease multiple sclerosis (MS) and its murine model experimental autoimmune encephalomyelitis (EAE). How TNF regulates disability during progressive disease remains unresolved. Using a progressive EAE model characterized by sustained TNF and increasing morbidity, this study evaluates the role of unregulated TNF in exacerbating central nervous system (CNS) pathology and inflammation.
methodsProgressive MS was mimicked by myelin oligodendrocyte glycoprotein (MOG) peptide immunization of mice expressing a dominant negative IFN-γ receptor alpha chain under the human glial fibrillary acidic protein promoter (GFAPγR1∆). Diseased GFAPγR1∆ mice were treated with anti-TNF or control monoclonal antibody during acute disease to monitor therapeutic effects on sustained disability, demyelination, CNS inflammation, and blood brain barrier (BBB) permeability.
resultsTNF was specifically sustained in infiltrating macrophages. Anti-TNF treatment decreased established clinical disability and mortality rate within 7 days. Control of disease progression was associated with a decline in myelin loss and leukocyte infiltration, as well as macrophage activation. In addition to mitigating CNS inflammation, TNF neutralization restored BBB integrity and enhanced CNS anti-inflammatory responses.
conclusionsSustained TNF production by infiltrating macrophages associated with progressive EAE exacerbates disease severity by promoting inflammation and disruption of BBB integrity, thereby counteracting establishment of an anti-inflammatory environment required for disease remission.
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