ArticleNature communications2023
RORγt-Raftlin1 complex regulates the pathogenicity of Th17 cells and colonic inflammation.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Serum profile of IL-29, IL-41, and raftlin in microvascular complications of type 2 diabetes mellitus.Scientific reports · 2026Article
- Dysregulated immunometabolism in gut inflammation.Acta biochimica et biophysica Sinica · 2026Review
- Elevated serum Raftlin levels in non-muscle invasive bladder cancer: diagnostic implications and rs690037 genotype analysis.Revista da Associacao Medica Brasileira (1992) · 2026Article
- The Potential Role of Microalgal Antioxidant Molecules on the Microbiota-Gut Axis in Inflammatory Bowel Diseases.Biomolecules · 2025Review
- Fine-tuning immunity: ubiquitin-dependent regulation of interleukin-17A expression by Th17 cells.Frontiers in immunology · 2025Review
- Review
- OLFM4 modulates intestinal inflammation by promoting IL-22Communications biology · 2024Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
Abstract
Th17 cells that produce Interleukin IL-17 are pathogenic in many human diseases, including inflammatory bowel disease, but are, paradoxically, essential for maintaining the integrity of the intestinal barrier in a non-inflammatory state. However, the intracellular mechanisms that regulate distinct transcriptional profiles and functional diversity of Th17 cells remain unclear. Here we show Raftlin1, a lipid raft protein, specifically upregulates and forms a complex with RORγt in pathogenic Th17 cells. Disruption of the RORγt-Raftlin1 complex results in the reduction of pathogenic Th17 cells in response to Citrobacter rodentium; however, there is no effect on nonpathogenic Th17 cells in response to commensal segmented filamentous bacteria. Mechanistically, we show that Raftlin1 recruits distinct phospholipids to RORγt and promotes the pathogenicity of Th17 cells. Thus, we have identified a mechanism that drives the pathogenic function of Th17 cells, which could provide a platform for advanced therapeutic strategies to dampen Th17-mediated inflammatory diseases.
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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.