ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
Itk signals promote neuroinflammation by regulating CD4+ T-cell activation and trafficking.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers.
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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.
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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
20 citing papers in PubMed, 40 citations in OpenAlex.
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- Inhibition of ITK Signaling Causes Amelioration in Sepsis-Associated Neuroinflammation and Depression-like State in Mice.International journal of molecular sciences · 2023Article
- Article
- A multi-network comparative analysis of whole-transcriptome and translatome reveals the effect of high-fat diet on APP/PS1 mice and the intervention with Chinese medicine.Frontiers in nutrition · 2022Article
- Targeting ITK signaling for T cell-mediated diseases.iScience · 2021Review
- Role of the IL-2 inducible tyrosine kinase ITK and its inhibitors in disease pathogenesis.Journal of molecular medicine (Berlin, Germany) · 2020Review
- Tuning T helper cell differentiation by ITK.Biochemical Society transactions · 2020Review
- CD8ImmunoHorizons · 2020Article
- ITK inhibition promotes long-term survival of cardiac allografts by regulating T cell PLCγ phosphorylation.American journal of translational research · 2020Article
- Non-receptor tyrosine kinase signaling in autoimmunity and therapeutic implications.Pharmacology & therapeutics · 2019Review
- Genetic Deficiency and Biochemical Inhibition of ITK Affect Human Th17, Treg, and Innate Lymphoid Cells.Journal of clinical immunology · 2019Article
- Interleukin-2-Inducible T-Cell Kinase Deficiency Impairs Early Pulmonary Protection AgainstFrontiers in immunology · 2019Article
- A negative role for the interleukin-2-inducible T-cell kinase (ITK) in human Foxp3+ TREG differentiation.PloS one · 2019Article
- Propofol Alters Long Non-Coding RNA Profiles in the Neonatal Mouse Hippocampus: Implication of Novel Mechanisms in Anesthetic-Induced Developmental Neurotoxicity.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2018Article
- Increased Levels of Pro-Inflammatory and Anti-Inflammatory Cellular Responses in Parkinson's Disease Patients: Search for a Disease Indicator.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
- Quantitative analysis of B-lymphocyte migration directed by CXCL13.Integrative biology : quantitative biosciences from nano to macro · 2016Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Here we demonstrate that interleukin-2-inducible T-cell kinase (Itk) signaling in cluster of differentiation 4-positive (CD4(+)) T cells promotes experimental autoimmune encephalomyelitis (EAE), the animal model of multiple sclerosis (MS). We show that Itk(-/-) mice exhibit reduced disease severity, and transfer of Itk(-/-) CD4(+) T cells into T cell-deficient recipients results in lower disease severity. We observed a significant reduction of CD4(+) T cells in the CNS of Itk(-/-) mice or recipients of Itk(-/-) CD4(+) T cells during EAE, which is consistent with attenuated disease. Itk(-/-) CD4(+) T cells exhibit defective response to myelin antigen stimulation attributable to displacement of filamentous actin from the CD4(+) coreceptor. This results in inadequate transmigration of Itk(-/-) CD4(+) T cells into the CNS and across brain endothelial barriers in vitro. Finally, Itk(-/-) CD4(+) T cells show significant reduction in production of T-helper 1 (Th1) and Th17 cytokines and exhibit skewed T effector/T regulatory cell ratios. These results indicate that signaling by Itk promotes autoimmunity and CNS inflammation, suggesting that it may be a viable target for treatment 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.