標題: Killer cell immunoglobulin-like receptors (KIR) and human leukocyte antigen-C (HLA-C) allorecognition patterns in women with endometriosis
作者: Chou, Ya-Ching
Chen, Chi-Huang
Chen, Ming-Jer
Chang, Ching-Wen
Chen, Pi-Hua
Yu, Mu-Hsien
Chen, Yi-Jen
Tsai, Eing-Mei
Yang, Peng-Sheng
Lin, Shyr-Yeu
Tzeng, Chii-Ruey
交大名義發表
生物科技學系
National Chiao Tung University
Department of Biological Science and Technology
公開日期: 17-Mar-2020
摘要: Endometriosis shares similarities with several autoimmune diseases. The human leukocyte antigen (HLA)-C genotype is associated with several human autoimmune diseases. HLA-C is a ligand of killer cell immunoglobulin receptors (KIRs) and is an essential regulator of natural killer cell activity, which is associated with endometriosis progression. Polymorphisms in HLA-C and KIR affect the activity of NK cells and susceptibility to several diseases. Therefore, we attempted to investigate an association between HLA-C genotype and KIR polymorphism and the occurrence of endometriosis. We tested the association of certain KIR and HLA-C combinations and the development of endometriosis by characterizing both KIR and HLA-C genes in 147 women with endometriosis and 117 controls. The HLA-C genotypes and KIR polymorphisms were analyzed via DNA-based method for higher-resolution genotyping. We found that the occurrence of HLA-C*03:03*01 was increased in endometriosis than in control groups. Analysis of various KIR haplotypes revealed differences between the endometriosis and control cohorts. The number of KIR centromeric A/A haplotypes was increased in the endometriosis group than controls. Moreover, the endometriosis cohort was characterized by reduced number of KIR2DS2-positive individuals in the Han Chinese population. Our current findings suggest that the KIR and HLA-C genotypes are associated with the pathogenesis of endometriosis.
URI: http://dx.doi.org/10.1038/s41598-020-61702-y
http://hdl.handle.net/11536/155468
ISSN: 2045-2322
DOI: 10.1038/s41598-020-61702-y
期刊: SCIENTIFIC REPORTS
Volume: 10
Issue: 1
起始頁: 0
結束頁: 0
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