ReviewCold Spring Harbor symposia on quantitative biology2015
Regulation of RORγt in Inflammatory Lymphoid Cell Differentiation.
Review in Cold Spring Harbor symposia on quantitative biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- The gut microbiome-bile acid-FXR interplay: a pivotal axis in metabolic and gastrointestinal diseases.Gut microbes · 2026Review
- Integrated RNA-seq and sQTL analysis reveal immune and splicing regulatory features underlying relapse and remission after treatment of Graves' disease.Frontiers in endocrinology · 2026Article
- The Role of ESS2/DGCR14: Is It an Essential Factor in Splicing and Transcription?International journal of molecular sciences · 2025Review
- Flow Cytometry Sorting of Memory CCR6Methods in molecular biology (Clifton, N.J.) · 2022Article
- Regenerating islet-derived protein (Reg)3β plays a crucial role in attenuation of ileitis and colitis in mice.Biochemistry and biophysics reports · 2020Article
- Myeloid Cell Hypoxia-Inducible Factors Promote Resolution of Inflammation in Experimental Colitis.Frontiers in immunology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
T-helper 17 (Th17) cells differentiate from naïve CD4(+) T cells in response to signals from commensal microbiota and produce cytokines critical for the integrity of mucosal barriers. These cells also disseminate throughout the body, and are key participants in numerous inflammatory processes. A key challenge is to elucidate the mechanisms that govern Th17 cell beneficial versus pathogenic functions, characterized by different cytokine profiles. Mucosal Th17 cells require the nuclear hormone receptor RORγt for their differentiation in draining lymph nodes. Cytokine expression is enabled in select tissues, to which these cells migrate, by external cues, such as the serum amyloid A proteins produced in response to commensal bacteria by epithelial cells in the small intestine. Additional cell-intrinsic cues contributing to production of Th17 cytokines during both homeostasis and inflammation include the RORγt-associated DEAD-box RNA helicase DDX5 and long noncoding RNA (lncRNA) Rmrp. The helicase activity of DDX5 is required for Rmrp-mediated assembly of the complex and colocalization with RORγt throughout the genome to regulate key Th17 genes. How these are regulated in diverse microenvironments may provide insights for therapeutic intervention in autoimmune disease.
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What OpenQuestion holds
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.