ArticleArthritis and rheumatism2008
Cytokines secreted in response to Toll-like receptor ligand stimulation modulate differentiation of human Th17 cells.
Article in Arthritis and rheumatism, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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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Who cites it
29 citing papers in PubMed, 57 citations in OpenAlex.
- Factors associated with circulating levels of IL-17A in a high HIV-burden population.Scientific reports · 2026Article
- Current perspective on biological properties of plasmacytoid dendritic cells and dysfunction in gut.Immunity, inflammation and disease · 2023Review
- The role of the gut microbiota and fecal microbiota transplantation in neuroimmune diseases.Frontiers in neurology · 2023Review
- Diminished HIV Infection of Target CD4+ T Cells in a Toll-Like Receptor 4 StimulatedFrontiers in immunology · 2019Article
- TLR7 Signaling Regulates Th17 Cells and Autoimmunity: Novel Potential for Autoimmune Therapy.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- TLRs, future potential therapeutic targets for RA.Autoimmunity reviews · 2017Review
- Prioritizing biological pathways by recognizing context in time-series gene expression data.BMC bioinformatics · 2016Article
- Factoring the intestinal microbiome into the pathogenesis of autoimmune hepatitis.World journal of gastroenterology · 2016Review
- Expression of TLR-7, MyD88, NF-kB, and INF-α in B Lymphocytes of Mayan Women with Systemic Lupus Erythematosus in Mexico.Frontiers in immunology · 2016Article
- Tetramers reveal IL-17-secreting CD4+ T cells that are specific for U1-70 in lupus and mixed connective tissue disease.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- The therapeutic potential of Rho kinase inhibitor fasudil derivative FaD-1 in experimental autoimmune encephalomyelitis.Journal of molecular neuroscience : MN · 2015Article
- Toll-like receptor mediated modulation of T cell response by commensal intestinal microbiota as a trigger for autoimmune arthritis.Journal of immunology research · 2015Review
- Engagement of Toll-like receptor 2 enhances interleukin (IL)-17(+) autoreactive T cell responses via p38 mitogen-activated protein kinase signalling in dendritic cells.Clinical and experimental immunology · 2014Article
- Interleukin-7 and Toll-like receptor 7 induce synergistic B cell and T cell activation.PloS one · 2014Article
- Expression and function of dectin-1 is defective in monocytes from patients with systemic lupus erythematosus and rheumatoid arthritis.Journal of clinical immunology · 2013Article
- Role of toll-like receptors in multiple sclerosis.American journal of clinical and experimental immunology · 2013Article
- Loss and dysregulation of Th17 cells during HIV infection.Clinical & developmental immunology · 2013Review
- T(H)1, T(H)2, and T(H)17 cells instruct monocytes to differentiate into specialized dendritic cell subsets.Blood · 2011Article
- Regulation of human Th9 differentiation by type I interferons and IL-21.Immunology and cell biology · 2010Article
- Modulation of immune responses through direct activation of Toll-like receptors to T cells.Clinical and experimental immunology · 2010Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTh17 cells (interleukin-17 [IL-17]-secreting T helper cells) have been implicated in the pathogenesis of rheumatoid arthritis and other autoimmune diseases, but the soluble factors that influence human Th17 differentiation have yet to be fully elucidated. This study was undertaken to investigate the hypothesis that the cytokines secreted by human peripheral blood mononuclear cells (PBMCs) in response to a subset of Toll-like receptor (TLR) ligands would influence Th17 polarization.
methodsSupernatants from human PBMCs treated with a panel of TLR agonists were tested for their ability to induce de novo IL-17 production in naive T helper cells. Multiplex cytokine analysis was used to identify candidate cytokines for subsequent blocking and sufficiency experiments.
resultsConditioned media from PBMCs stimulated with TLR-4 or TLR-8/7 agonists, but not from those stimulated with TLR-2/1, -3, or -9 agonists, evoked robust secretion of IL-17 by T helper cells, independent of coculture with antigen-presenting cells. Multiplex analysis of 22 cytokines and chemokines identified a 6-factor cytokine signature that significantly correlated with IL-17-inducing activity. T cell activation in the presence of recombinant IL-1beta, IL-6, and IL-23 reconstituted robust IL-17 production, and this was enhanced by transforming growth factor beta (TGFbeta). IL-6 suppressed the expression of forkhead box P3 and reversed TGFbeta-mediated inhibition of T cell proliferation, but did not trigger IL-17 secretion. IL-17 production was completely abrogated by anti-IL-1 or IL-1 receptor antagonist and partially inhibited by anti-IL-6, anti-IL-2, or exogenous retinoic acid, but not by anti-tumor necrosis factor alpha. IL-1beta and IL-6 independently induced IL-21 secretion, but the presence of IL-21 alone was not sufficient for IL-17 production.
conclusionThese results indicate that ligation of a subset of TLRs generates proinflammatory cytokines that combine to potentiate human Th17 differentiation.
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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.