ArticleJournal of immunology (Baltimore, Md. : 1950)2014
Regulation of experimental autoimmune encephalomyelitis by TPL-2 kinase.
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 25 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
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Who cites it
25 citing papers in PubMed, 38 citations in OpenAlex.
- MAP3K8 is a potential therapeutic target in airway epithelial inflammation.Journal of inflammation (London, England) · 2024Article
- Article
- ERK1/2 in immune signalling.Biochemical Society transactions · 2022Review
- TPL-2 Inhibits IFN-β Expression via an ERK1/2-TCF-FOS Axis in TLR4-Stimulated Macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Trends in kinase drug discovery: targets, indications and inhibitor design.Nature reviews. Drug discovery · 2021Review
- TPL-2 kinase induces phagosome acidification to promote macrophage killing of bacteria.The EMBO journal · 2021Article
- Kinase inhibition in autoimmunity and inflammation.Nature reviews. Drug discovery · 2021Review
- Tumor progression locus 2 (TPL2) in tumor-promoting Inflammation, Tumorigenesis and Tumor Immunity.Theranostics · 2020Review
- Tpl2 is required for VEGF-A-stimulated signal transduction and endothelial cell function.Biology open · 2019Article
- ABIN2 Function Is Required To Suppress DSS-Induced Colitis by a Tpl2-Independent Mechanism.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- A20-binding inhibitor of NF-κB (ABIN) 2 negatively regulates allergic airway inflammation.The Journal of experimental medicine · 2018Article
- Assaying kinase activity of the TPL-2/NF-κB1 p105/ABIN-2 complex using an optimal peptide substrate.The Biochemical journal · 2018Article
- Tpl2 Promotes Innate Cell Recruitment and Effector T Cell Differentiation To Limit Citrobacter rodentium Burden and Dissemination.Infection and immunity · 2017Article
- TPL-2 restricts Ccl24-dependent immunity to Heligmosomoides polygyrus.PLoS pathogens · 2017Article
- Tumor progression locus 2 reduces severe allergic airway inflammation by inhibiting Ccl24 production in dendritic cells.The Journal of allergy and clinical immunology · 2017Article
- AGut · 2016Article
- TLR and TNF-R1 activation of the MKK3/MKK6-p38α axis in macrophages is mediated by TPL-2 kinase.The Biochemical journal · 2016Article
- Tumor Progression Locus 2 (Tpl2) Activates the Mammalian Target of Rapamycin (mTOR) Pathway, Inhibits Forkhead Box P3 (FoxP3) Expression, and Limits Regulatory T Cell (Treg) Immunosuppressive Functions.The Journal of biological chemistry · 2016Article
- TPL-2 Regulates Macrophage Lipid Metabolism and M2 Differentiation to Control TH2-Mediated Immunopathology.PLoS pathogens · 2016Article
- TPL2 mediates IL-17R signaling in neuroinflammation.Oncotarget · 2015Article
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 4 countries.
Funding
Abstract
Tumor progression locus 2 (TPL-2) expression is required for efficient polarization of naive T cells to Th1 effector cells in vitro, as well as for Th1-mediated immune responses. In the present study, we investigated the potential role of TPL-2 in Th17 cells. TPL-2 was found to be dispensable for Th17 cell differentiation in vitro, and for the initial priming of Th17 cells in experimental autoimmune encephalomyelitis (EAE), a Th17 cell-mediated disease model for multiple sclerosis. Nevertheless, TPL-2-deficient mice were protected from EAE, which correlated with reduced immune cell infiltration, demyelination, and axonal damage in the CNS. Adoptive transfer experiments demonstrated that there was no T cell-intrinsic function for TPL-2 in EAE, and that TPL-2 signaling was not required in radiation-sensitive hematopoietic cells. Rather, TPL-2 signaling in radiation-resistant stromal cells promoted the effector phase of the disease. Importantly, using a newly generated mouse strain expressing a kinase-inactive form of TPL-2, we demonstrated that stimulation of EAE was dependent on the catalytic activity of TPL-2 and not its adaptor function to stabilize the associated ubiquitin-binding protein ABIN-2. Our data therefore raise the possibility that small molecule inhibitors of TPL-2 may be beneficial in multiple sclerosis therapy.
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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.