ArticleJournal of immunology (Baltimore, Md. : 1950)2014
Cytokine-regulated neutrophil recruitment is required for brain but not spinal cord inflammation during experimental autoimmune encephalomyelitis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
60 citing papers in PubMed, 84 citations in OpenAlex.
- Microglia and border-associated macrophages play opposite roles in cerebrovascular and leukocyte responses under systemic inflammation in male mice.Nature communications · 2026Article
- Single-cell RNA sequencing uncovers neutrophil clusters associated with autoimmune neuroinflammation.Journal of neuroinflammation · 2026Article
- Single-Cell RNA Sequencing Uncovers Neutrophil Clusters Associated with Autoimmune Neuroinflammation.Research square · 2025Article
- TScience advances · 2025Article
- Neutrophils, NETs and multiple sclerosis: a mini review.Frontiers in immunology · 2025Review
- Protective effect of TCR-mediated MAIT cell activation during experimental autoimmune encephalomyelitis.Nature communications · 2024Article
- RIPK3 promotes brain region-specific interferon signaling and restriction of tick-borne flavivirus infection.PLoS pathogens · 2023Article
- Astrocyte interferon-gamma signaling dampens inflammation during chronic central nervous system autoimmunity via PD-L1.Journal of neuroinflammation · 2023Article
- Neutrophil biology in injuries and diseases of the central and peripheral nervous systems.Progress in neurobiology · 2023Review
- The role of neuroinflammation in the transition of acute to chronic pain and the opioid-induced hyperalgesia and tolerance.Frontiers in pharmacology · 2023Review
- B Cells Drive MHC Class I-Restricted CD4 T Cells to Induce Spontaneous Central Nervous System Autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- The antimicrobial peptide cathelicidin drives development of experimental autoimmune encephalomyelitis in mice by affecting Th17 differentiation.PLoS biology · 2022Article
- Levetiracetam Suppresses the Infiltration of Neutrophils and Monocytes and Downregulates Many Inflammatory Cytokines during Epileptogenesis in Pilocarpine-Induced Status Epilepticus Mice.International journal of molecular sciences · 2022Article
- The Importance of CXCL1 in Physiology and Noncancerous Diseases of Bone, Bone Marrow, Muscle and the Nervous System.International journal of molecular sciences · 2022Review
- Neuroinflammation and Neutrophils: Modulation by Ouabain.Frontiers in pharmacology · 2022Review
- Obesity induced gut dysbiosis contributes to disease severity in an animal model of multiple sclerosis.Frontiers in immunology · 2022Article
- Sustained Infiltration of Neutrophils Into the CNS Results in Increased Demyelination in a Viral-Induced Model of Multiple Sclerosis.Frontiers in immunology · 2022Article
- mScience advances · 2021Article
- Pertussis Toxin Inhibits Encephalitogenic T-Cell Infiltration and Promotes a B-Cell-Driven Disease during Th17-EAE.International journal of molecular sciences · 2021Article
- Modulation of PKM activity affects the differentiation of TScience signaling · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Multiple sclerosis (MS) is an autoimmune disease in which inflammatory lesions lead to tissue injury in the brain and/or spinal cord. The specific sites of tissue injury are strong determinants of clinical outcome in MS, but the pathways that determine whether damage occurs in the brain or spinal cord are not understood. Previous studies in mouse models of MS demonstrated that IFN-γ and IL-17 regulate lesion localization within the brain; however, the mechanisms by which these cytokines mediate their effects have not been identified. In the present study, we show that IL-17 promoted, but IFN-γ inhibited, ELR(+) chemokine-mediated neutrophil recruitment to the brain, and that neutrophil infiltration was required for parenchymal tissue damage in the brain. In contrast, IFN-γ promoted ELR(+) chemokine expression and neutrophil recruitment to the spinal cord. Surprisingly, tissue injury in the spinal cord did not exhibit the same dependence on neutrophil recruitment that was observed for the brain. Our results demonstrate that the brain and spinal cord exhibit distinct sensitivities to cellular mediators of tissue damage, and that IL-17 and IFN-γ differentially regulate recruitment of these mediators to each microenvironment. These findings suggest an approach toward tailoring therapies for patients with distinct patterns of neuroinflammation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.