Association of CTLA-4 polymorphisms with increased risks of myasthenia gravis
Association of CTLA-4 polymorphisms with increased risks of myasthenia gravis
Li et al., 2018 | Ann Hum Genet | Meta Analysis
Citation
Li Fang, Yuan Wuzhou, Wu Xiushan. Association of CTLA-4 polymorphisms with increased risks of myasthenia gravis. Ann Hum Genet. 2018-Nov;82(6):358-369. doi:10.1111/ahg.12262
Abstract
Myasthenia gravis (MG) is considered to be a kind of autoimmune disorder resulting from dysfunction of neuromuscular transmission caused by autoantibodies against the nicotinic acetylcholine receptors. A number of studies have identified Cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4) as a candidate gene for MG. Several recent reports have indicated that single nucleotide polymorphisms (SNPs) of CTLA-4, including rs733618, rs4553808, rs5742909, rs231775, and rs3087243 were associated with the risks of MG; however, the results were not consistent. To assess the correlations between CTLA-4 SNPs and MG susceptibility, a meta-analysis was performed following a series of database searching. A total of 1460 cases and 1652 controls from 12 studies were enrolled in the analysis. Our results indicated that rs231775 and rs733618 were associated with higher risks of MG, providing potential references for future case-control studies.
Key Findings
Our results indicated that rs231775 and rs733618 were associated with higher risks of MG, providing potential references for future case-control studies.
Outcomes Measured
- Requires manual extraction
Population
| Field | Value |
|---|---|
| Population | See abstract |
| Sample Size | 12 |
| Age Range | See abstract |
| Condition | See abstract |
MeSH Terms
- CTLA-4 Antigen
- Genetic Predisposition to Disease
- Humans
- Myasthenia Gravis
- Polymorphism, Single Nucleotide
- Risk Factors
Evidence Classification
- Level: Meta Analysis
- Publication Types: Journal Article, Meta-Analysis, Research Support, Non-U.S. Gov't
- Vertical: niacin
Provenance
- PMID: 30009380
- DOI: 10.1111/ahg.12262
- PMCID: Not in PMC
- Verified: 2026-04-09 via PubMed E-utilities API
Source extracted via PubMed E-utilities API on 2026-04-09