ArticleScientific reports2017
Common variants of T-cells contribute differently to phenotypic variation in sarcoidosis.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
What it found
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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
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- Sarcoidosis as an Autoimmune Disease.Frontiers in immunology · 2019Pooled it
- Immunopathogenesis of Sarcoidosis.Seminars in respiratory and critical care medicine · 2025Review
- Sarcoidosis in the Genomic Era: From Genetic Drivers to Tailored Therapies.Current allergy and asthma reports · 2025Review
- SHP2 promotes sarcoidosis severity by inhibiting SKP2-targeted ubiquitination of TBET in CD8Science translational medicine · 2023Article
- Lymphocyte Subsets and Pulmonary Nodules to Predict the Progression of Sarcoidosis.Biomedicines · 2023Article
- CD31Journal of thoracic disease · 2021Article
- Recent advances in sarcoidosis genomics: epigenetics, gene expression, and gene by environment (G × E) interaction studies.Current opinion in pulmonary medicine · 2020Review
- Management of chronic ocular sarcoidosis: challenges and solutions.Clinical ophthalmology (Auckland, N.Z.) · 2018Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The involvement of the immune system, particularly the role of T-cells, in sarcoidosis is unclear. The existence of higher CD4+ T-cells and increased CD4/CD8 ratio may indicate a pathogenic role of T-cells in the disease. In this study, we quantified the contribution of T-cells associated variants and of CD4/CD8 ratio in sarcoidosis phenotypes, Löfgren's syndrome (LS) and non- Löfgren's syndrome (non-LS). We employed a polygenic-based approach using genome-wide association studies results on relative levels of T-cells in healthy individuals to measure the genetic contribution of T-cells in sarcoidosis entities. Results revealed that the genetic architecture of LS is highly influenced by genetic variants associated with CD8+ T-cells and CD4/CD8 ratio, explaining up to 7.94% and 6.49% of LS variation, respectively; whereas, the genetic architecture of non-LS is minimally influenced by T-cells, explaining a phenotypic variation of <1%. Moreover, pleiotropy assessment between T-cells and LS/non-LS associated-variants led to the discovery of highly scored pathway maps that shared common factors related to antigen presentation and T-cell regulatory mechanisms. Differences in significant polygenic scores, presence of pleiotropy, and distinct genetic factors provide further insights on how genetic variants and genes associated with relative levels of T-cell subtypes contribute differently to sarcoidosis phenotypes.
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Registered trials
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