ArticleTransplant international : official journal of the European Society for Organ Transplantation2008
In primed allo-tolerance, TIM-3-Ig rapidly suppresses TGFbeta, but has no immediate effect on Foxp3.
Article in Transplant international : official journal of the European Society for Organ Transplantation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 7 citations in OpenAlex.
- Concurrent Chemoradiotherapy Increases the Levels of Soluble Immune Checkpoint Proteins in Patients with Locally Advanced Cervical Cancer.Journal of immunology research · 2022Article
- Soluble TIM3 and Its Ligands Galectin-9 and CEACAM1 Are in Disequilibrium During Alcohol-Related Liver Disease and Promote Impairment of Anti-bacterial Immunity.Frontiers in physiology · 2021Article
- Article
- The role of coinhibitory signaling pathways in transplantation and tolerance.Frontiers in immunology · 2012Article
- The emerging role of the TIM molecules in transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
T-cell immunoglobulin mucin-3 (TIM-3) is only expressed by differentiated TH1 cells following their proliferative response to antigen, functioning to terminate TH1-mediated immunity upon binding to the TIM-3 ligand, galectin-9. This critical regulatory process involves Treg cells via their stable expression of galectin-9. Soluble TIM-3-Ig blocks galectin-9 and prevents induction of peripheral tolerance. Here we have looked for evidence that TIM-3-Ig might also break established regulatory tolerance. Using allo-primed spleen cells cultured ex vivo and challenged with irradiated donor-type stimulator cells either alone or together with 20 microg/ml TIM-3-Ig, we measured daily cytokine release [IL2, inferon gamma (INFgamma), transforming growth factor beta (TGFbeta), IL6, IL10] and cellular Foxp3 protein. In allo-tolerance, a specific effect of TIM-3-Ig was some fourfold reduction in TGFbeta. Foxp3 was induced in the allo-tolerant response to donor and this was not altered by TIM-3-Ig over the 5-day culture period. No Foxp3 was detected in either rejected or donor stimulator cells at any time. Thus, in an ex vivo model of in vivo tolerance to heart allografts, TIM-3-Ig therapy appears to reduce the stable tolerogenic environment by a rapid and specific repression of TGFbeta release.
Indexed as
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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.