ReviewJournal of clinical immunology2014
Unexpected targets and triggers of autoimmunity.
Review in Journal of clinical immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 14 citations in OpenAlex.
- Characterizing the Interplay of Lymphocytes in Graves' Disease.International journal of molecular sciences · 2023Review
- Article
- A Simple and Robust Protocol forBio-protocol · 2021Article
- Article
- Tacrolimus inhibits Th1 and Th17 responses in MuSK-antibody positive myasthenia gravis patients.Experimental neurology · 2019Article
- Article
- miR-155-3p Drives the Development of Autoimmune Demyelination by Regulation of Heat Shock Protein 40.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Article
- Feedback inhibition of CREB signaling promotes beta cell dysfunction in insulin resistance.Cell reports · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Recent findings indicate that the role of Th17 cells in the pathogenesis of tissue inflammation and autoimmunity has become rather complicated. While interleukin-17 (IL-17) producing CD4+ T cells are found frequently within the peripheral target tissue during the course of autoimmune disease, these cells may contribute to or protect from inflammation. Accumulating reports have revealed the existence of both pathogenic and non-pathogenic Th17 cells. These Th17 subsets produce the signature cytokines IL-17A and IL-17F yet have distinct and divergent roles in inducing autoimmune tissue inflammation. Comparative genomic sequence analyses between the pathogenic and non-pathogenic Th17 cells have exposed unexpected and extensive population heterogeneity within the Th17 subset. Here we review some of the unexpected factors that may drive pathogenic divergence. Understanding the functional consequences of Th17 cell diversity may allow for the selection of more precise targets for intervention in autoimmune and inflammatory diseases.
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Identifiers
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.