ArticleFrontiers in immunology2019
Association of Functional Polymorphisms of KIR3DL1/DS1 With Behçet's Disease.
Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- The Role of Killer Ig-like Receptors in Diseases from A to Z.International journal of molecular sciences · 2025Review
- Widespread venous thrombosis: Unveiling a complex case of Behçet's disease with a literature perspective.Open medicine (Warsaw, Poland) · 2025Article
- Article
- Frail Silk: Is the Hughes-Stovin Syndrome a Behçet Syndrome Subtype with Aneurysm-Involved Gene Variants?International journal of molecular sciences · 2023Review
- Successful treatment of a refractory intestinal Behcet's disease with an oncology history by Vedolizumab: a case report and literature review.Frontiers in immunology · 2023Review
- HLA-E restricted cytomegalovirus UL40 peptide polymorphism may represent a risk factor following congenital infection.BMC genomics · 2022Article
- The association of Behçet's syndrome with HLA-B51 as understood in 2021.Current opinion in rheumatology · 2022Review
- A comprehensive genome-wide analysis of long non-coding RNA and mRNA expression profiles of JAK2V617F-positive classical myeloproliferative neoplasms.Bioengineered · 2021Article
- A Contemporary Review of Behcet's Syndrome.Clinical reviews in allergy & immunology · 2021Review
- Article
- Current research status of HLA in immune-related diseases.Immunity, inflammation and disease · 2021Review
- Pathogenesis of Non-Infectious Uveitis Elucidated by Recent Genetic Findings.Frontiers in immunology · 2021Review
- Haplotype-Based Analysis ofFrontiers in immunology · 2020Article
- Past and Present Behçet's Disease Animal Models.Current drug targets · 2020Review
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Authors and funding
21 authors at 19 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Behçet's disease (BD) is an immune-mediated vasculitis related to imbalances between the innate and adaptive immune response. Infectious agents or environmental factors may trigger the disease in genetically predisposed individuals. HLA-B51 is the genetic factor stronger associated with the disease, although the bases of this association remain elusive. NK cells have also been implicated in the etiopathogenesis of BD. A family of NK receptors, Killer-cell Immunoglobulin-like Receptor (KIR), with a very complex organization, is very important in the education and control of the NK cells by the union to their ligands, most of them, HLA class I molecules. This study aimed to investigate the contribution of certain KIR functional polymorphisms to the susceptibility to BD. A total of 466 BD patients and 444 healthy individuals were genotyped in HLA class I (A, B, and C). The set of KIR genes and the functional variants of KIR3DL1/DS1 and KIR2DS4 were also determined. Frequency of KIR3DL1
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