ArticleJournal of immunology (Baltimore, Md. : 1950)2009
Unlike Th1, Th17 cells mediate sustained autoimmune inflammation and are highly resistant to restimulation-induced cell death.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 58 citations in OpenAlex.
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- AI-Driven Analysis Unveils Functional Dynamics of Müller Cells in Retinal Autoimmune Inflammation.bioRxiv : the preprint server for biology · 2025Article
- OXPHOS promotes apoptotic resistance and cellular persistence in TScience immunology · 2022Article
- The Th1 cell regulatory circuitry is largely conserved between human and mouse.Life science alliance · 2021Article
- T cell plasticity in renal autoimmune disease.Cell and tissue research · 2021Review
- TCDD attenuates EAE through induction of FasL on B cells and inhibition of IgG production.Toxicology · 2021Article
- FOXP3 protects conventional human T cells from premature restimulation-induced cell death.Cellular & molecular immunology · 2021Article
- Emerging Role of Adipocyte Dysfunction in Inducing Heart Failure Among Obese Patients With Prediabetes and Known Diabetes Mellitus.Frontiers in cardiovascular medicine · 2020Review
- Neuroinflammation and B-Cell Phenotypes in Cervical and Lumbosacral Regions of the Spinal Cord in Experimental Autoimmune Encephalomyelitis in the Absence of Pertussis Toxin.Neuroimmunomodulation · 2019Article
- Unlike Th1/Th17 cells, Th2/Th9 cells selectively migrate to the limbus/conjunctiva and initiate an eosinophilic infiltration process.Experimental eye research · 2018Article
- Loss ofFrontiers in immunology · 2018Article
- Ocular antigen does not cause disease unless presented in the context of inflammation.Scientific reports · 2017Article
- Shedding New Light on the Process of "Licensing" for Pathogenicity by Th Lymphocytes.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Th1 and Th17 Cells and Associated Cytokines Discriminate among Clinically Isolated Syndrome and Multiple Sclerosis Phenotypes.Frontiers in immunology · 2017Article
- Article
- Boosting BCG-primed responses with a subunit Apa vaccine during the waning phase improves immunity and imparts protection against Mycobacterium tuberculosis.Scientific reports · 2016Article
- Digoxin Inhibits Induction of Experimental Autoimmune Uveitis in Mice, but Causes Severe Retinal Degeneration.Investigative ophthalmology & visual science · 2016Article
- Cutting Edge: IL-1 Receptor Signaling is Critical for the Development of Autoimmune Uveitis.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Fas-Fas Ligand: Checkpoint of T Cell Functions in Multiple Sclerosis.Frontiers in immunology · 2016Review
- IL-7/IL-7 Receptor Signaling Differentially Affects Effector CD4+ T Cell Subsets Involved in Experimental Autoimmune Encephalomyelitis.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Both Th1 and Th17 T cell subsets can mediate inflammation, but the kinetics of the pathogenic processes mediated by these two subsets have not been investigated. Using an experimental system in which TCR-transgenic Th1 or Th17 cells specific for hen egg lysozyme induce ocular inflammation in recipient mice expressing eye-restricted hen egg lysozyme, we found important differences in the in vivo behavior of these two subsets. Th1 cells initially proliferated considerably faster and invaded the eye more quickly than their Th17 counterparts, but then disappeared rapidly. By contrast, Th17 cells accumulated and remained the majority of the infiltrating CD4(+) cells in the eye for as long as 25 days after transfer, mediating more long-lasting pathological changes. Unlike Th1, Th17 cells were highly resistant to restimulation-induced apoptosis, a major pathway by which autoimmune and chronically restimulated Th1 cells are eliminated. Th17 cells had reduced Fas ligand production and resistance to Fas-induced apoptosis, relative to Th1 cells, despite similar surface expression of Fas. Th17-induced ocular inflammation also differed from Th1-induced inflammation by consisting of more neutrophils, whereas Th1-induced disease had higher proportions of CD8 cells. Taken together, our data show that pathogenic processes triggered by Th17 lag behind those induced by Th1, but then persist remarkably longer, apparently due to the relative resistance of Th17 cells to restimulation-induced cell death. The long-lasting inflammation induced by Th17 cells is in accord with these cells being involved in chronic conditions in humans.
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