ArticleScientific reports2017
Ndfip1 restricts Th17 cell potency by limiting lineage stability and proinflammatory cytokine production.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- [Ubiquitination-mediated regulation of T cell homeostasis and autoimmune diseases].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Review
- Fine-tuning immunity: ubiquitin-dependent regulation of interleukin-17A expression by Th17 cells.Frontiers in immunology · 2025Review
- RORγt protein modifications and IL-17-mediated inflammation.Trends in immunology · 2021Review
- The Ubiquitin-Proteasome System in Immune Cells.Biomolecules · 2021Review
- ITCH as a potential therapeutic target in human cancers.Seminars in cancer biology · 2020Review
- Itch attenuates CD4 T-cell proliferation in mice by limiting WBP2 protein stability.European journal of immunology · 2020Article
- Collagenous Colitis Is Associated With HLA Signature and Shares Genetic Risks With Other Immune-Mediated Diseases.Gastroenterology · 2020Article
- Itch regulation of innate and adaptive immune responses in mice and humans.Journal of leukocyte biology · 2020Review
- Effector TCell · 2019Article
- Immune regulation by protein ubiquitination: roles of the E3 ligases VHL and Itch.Protein & cell · 2019Review
- Regulation of autoimmune disease by the E3 ubiquitin ligase Itch.Cellular immunology · 2019Review
- Ndfip Proteins Target Robo Receptors for Degradation and Allow Commissural Axons to Cross the Midline in the Developing Spinal Cord.Cell reports · 2019Article
- The Ubiquitin Ligase Adaptor NDFIP1 Selectively Enforces a CD8Cell reports · 2018Article
- Ndfip1 restricts mTORC1 signalling and glycolysis in regulatory T cells to prevent autoinflammatory disease.Nature communications · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
While Th17 cells can protect against colonization by pathogenic organisms, they also have the potential to become pathogenic and promote autoimmune and inflammatory diseases. Mechanisms that control their pathogenic potential remain poorly understood. Here we show that Ndfip1, a co-activator of the E3 ubiquitin ligase Itch, restricts the frequency and pathogenicity of Th17 cells. Mice lacking Ndfip1 have increased numbers of Th17 cells, and this increase is cell intrinsic. We found that Ndfip1 restricts production of the proinflammatory cytokines in Th17 cells. Increased cytokine production correlated with reduced degradation and accumulation of RORγT. When transferred in vivo, Th17 cells lacking Ndfip1 were more likely to maintain their ability to make IL-17, were more potent proinflammatory cytokine producers, and were powerful inducers of colitis. Together our data support an essential role for Ndfip1 in degrading RORγT and suppressing Th17 lineage stability, proinflammatory cytokine production, and pathogenicity.
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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.