ArticleClinical and translational medicine2025
CD31 regulates metabolic switch in Treg migration attenuates rheumatoid arthritis.
Article in Clinical and translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Hyodeoxycholic acid attenuates atherosclerosis by antagonizing FXR and modulating the PD-1/mTORC1 signaling axis.Redox biology · 2026Article
- Immunometabolic dysregulation in autoimmune rheumatic diseases: the central role of glycolytic reprogramming in pathogenesis and traditional Chinese medicine therapy.Frontiers in immunology · 2026Review
- CD31 regulates metabolic switch in Treg migration attenuates rheumatoid arthritis.Clinical and translational medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
CD31 (PECAM-1) plays a critical role in T cell migration, whilst its immunoreceptor tyrosine inhibitory motifs (ITIMs), Y663 and Y686, are recognised for their roles in endothelial function, the precise mechanism in regulating immune cell remains elusive. Here, we demonstrate that CD31 is essential for Treg migration. Upon ITIM engagement, CD31 activates and interacts with the protein tyrosine phosphatase SHP2. In vivo, CD31 Y663F gene transfer recapitulates the wild-type migration phenotype, driven by a metabolic switch to fructose utilisation under the regulation of the PFKFB3 gene. Conversely, the Y686F mutation impairs Tregs migration by disrupting both glycolysis and the switch to fructose metabolism, thus promoting the mitochondrial function via activation of the RNF111/OGT pathway. Our findings reveal a novel role for CD31 ITIMs in orchestrating a metabolic that is switch crucial for Treg migration. This understanding of CD31 polymorphisms and their impact on Treg migration offers potential therapeutic avenues for autoimmune diseases, particularly rheumatoid arthritis (RA). KEY POINTS: CD31 Y663F-mutant Tregs exhibit a glucose-to-fructose metabolic shift, characterised by reduced glucose uptake and enhanced fructose utilisation regulated by PFKFB3. CD31 Y686F mutation disrupts both glycolysis and fructose metabolism in Tregs, shifting energy production towards mitochondrial function via the RNF111/OGT pathway. These findings highlight a novel mechanism by which CD31 ITIMs control Treg migration, offering new therapeutic targets for autoimmune diseases such as RA.
Indexed as
Identifiers
What Socratic 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 Socratic graph.