Trial reportJournal of immunology (Baltimore, Md. : 1950)2012
CCR2(+)CCR5(+) T cells produce matrix metalloproteinase-9 and osteopontin in the pathogenesis of multiple sclerosis.
Trial report in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 79 citations in OpenAlex.
- Failed immune responses across multiple pathologies share pan-tumor and circulating lymphocytic targets.The Journal of clinical investigation · 2019Trial
- PINK1 deficiency rewires early immune responses in a mouse model of Parkinson's disease triggered by intestinal infection.NPJ Parkinson's disease · 2025Article
- Migration arrest and transendothelial trafficking of human pathogenic-like Th17 cells are mediated by differentially positioned chemokines.Nature communications · 2025Article
- Engineered immunological niche directs therapeutic development in models of progressive multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Multiple Sclerosis Patient Macrophages Impaired Metabolism Leads to an Altered Response to Activation Stimuli.Neurology(R) neuroimmunology & neuroinflammation · 2024Article
- Whole-Body Cryostimulation in Multiple Sclerosis: A Scoping Review.Journal of clinical medicine · 2024Article
- Effect of Whole-Body Cryotherapy on Oxidant-Antioxidant Imbalance in Women with Multiple Sclerosis.Journal of clinical medicine · 2023Article
- Microglial expression of CD83 governs cellular activation and restrains neuroinflammation in experimental autoimmune encephalomyelitis.Nature communications · 2023Article
- High levels of endothelial ICAM-1 prohibit natalizumab mediated abrogation of CD4Journal of neuroinflammation · 2023Article
- Immune Profiling Reveals the T-Cell Effect of Ocrelizumab in Early Relapsing-Remitting Multiple Sclerosis.Neurology(R) neuroimmunology & neuroinflammation · 2023Article
- Chemokine positioning determines mutually exclusive roles for their receptors in extravasation of pathogenic human T cells.bioRxiv : the preprint server for biology · 2023Article
- Differential effects of anti-CD20 therapy on CD4 and CD8 T cells and implication of CD20-expressing CD8 T cells in MS disease activity.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- CD4Journal of neuroinflammation · 2022Article
- Chemokine-Driven Migration of Pro-Inflammatory CD4Frontiers in immunology · 2022Review
- Two dimensional nanosheets as immunoregulator improve HIV vaccine efficacy.Chemical science · 2021Article
- Dual CCR5/CCR2 targeting: opportunities for the cure of complex disorders.Cellular and molecular life sciences : CMLS · 2019Review
- Matrix Metalloproteinase 9 and Osteopontin Interact to Support Synaptogenesis in the Olfactory Bulb after Mild Traumatic Brain Injury.Journal of neurotrauma · 2019Article
- Abnormal effector and regulatory T cell subsets in paediatric-onset multiple sclerosis.Brain : a journal of neurology · 2019Article
- Functional Change of Effector Tumor-Infiltrating CCR5Frontiers in immunology · 2019Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is a demyelinating disease of the CNS that is presumably mediated by CD4(+) autoimmune T cells. Although both Th1 and Th17 cells have the potential to cause inflammatory CNS pathology in rodents, the identity of pathogenic T cells remains unclear in human MS. Given that each Th cell subset preferentially expresses specific chemokine receptors, we were interested to know whether T cells defined by a particular chemokine receptor profile play an active role in the pathogenesis of MS. In this article, we report that CCR2(+)CCR5(+) T cells constitute a unique population selectively enriched in the cerebrospinal fluid of MS patients during relapse but not in patients with other neurologic diseases. After polyclonal stimulation, the CCR2(+)CCR5(+) T cells exhibited a distinct ability to produce matrix metalloproteinase-9 and osteopontin, which are involved in the CNS pathology of MS. Furthermore, after TCR stimulation, the CCR2(+)CCR5(+) T cells showed a higher invasive potential across an in vitro blood-brain barrier model compared with other T cells. Of note, the CCR2(+)CCR5(+) T cells from MS patients in relapse are reactive to myelin basic protein, as assessed by production of IFN-γ. We also demonstrated that the CCR6(-), but not the CCR6(+), population within CCR2(+)CCR5(+) T cells was highly enriched in the cerebrospinal fluid during MS relapse (p < 0.0005) and expressed higher levels of IFN-γ and matrix metalloproteinase-9. Taken together, we propose that autoimmune CCR2(+)CCR5(+)CCR6(-) Th1 cells play a crucial role in the pathogenesis of MS.
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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.