SynthesisBioscience reports2018
TIM-3 rs1036199 polymorphism increases susceptibility to autoimmune diseases: evidence based on 4200 subjects.
Synthesis in Bioscience reports, 2018. 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, 12 citations in OpenAlex.
- PD-1, BTLA and TIGIT as therapeutic targets for rheumatic disease.Nature reviews. Rheumatology · 2026Review
- The role of the TIM-3 receptor in inflammatory bowel disease and autoimmunity: implications for TIM-3 and TCR crosstalk.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Autoimmunity and Carcinogenesis: Their Relationship under the Umbrella of Autophagy.Biomedicines · 2023Review
- Autoimmunity and Cancer-Two Sides of the Same Coin.Frontiers in immunology · 2022Review
- TIM-3 Genetic Variants Are Associated with Altered Clinical Outcome and Susceptibility to Gram-Positive Infections in Patients with Sepsis.International journal of molecular sciences · 2020Article
- Immune Checkpoint Molecules-Inherited Variations as Markers for Cancer Risk.Frontiers in immunology · 2020Review
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Conflicting results have been reported regarding differing studies on the association between T-cell immunoglobulin and mucin domain 3 polymorphisms and autoimmune disease. The purpose of the present study was to evaluate the association of TIM-3 rs1036199 (4259 G/T) polymorphism with autoimmune disease susceptibility. A meta-analysis was performed to obtain a more precise evaluation of the association. Ten eligible studies were retrieved by searching PubMed, Embase and Web of Science databases, and statistical analyses were performed using STATA software. The pooled results indicated that TIM-3 rs1036199 polymorphism was significantly associated with an increased risk of overall autoimmune disease in allele comparison (G versus T: OR = 1.59, 95%CI: 1.17-2.17) and heterozygous comparison (GT versus TT: OR = 1.68, 95%CI: 1.37-2.06). Subgroup analyses based on disease type demonstrated that TIM-3 rs1036199 polymorphism was associated with an increased risk of rheumatic arthritis (G versus T: OR = 1.88, 95%CI: 1.45-2.44; GT versus TT: OR = 2.02, 95%CI: 1.53-2.65), especially in Asian populations.
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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.