CD86 +1057G/A polymorphism and risk of chronic immune thrombocytopenia. (November 2014)

• Record Type: Journal Article
• Authors: Wu, Pin; Wang, Zhi; Lu, Shiyun; Zhao, Xiaohong
• Is Part Of: Autoimmunity. Volume 47:Number 7(2014)
• Page Start: 482
• Page End: 485
• Publication Date: 2014-11
• Subjects: Autoimmunity -- Periodicals; Autoimmune diseases -- Periodicals; 571.973
• DOI: 10.3109/08916934.2014.921813
• Languages: English
• ISSNs: 0891-6934

Abstract

<abstract> <title>Abstract</title> <p>The G to A transition at position +1057 single nucleotide polymorphism site in <italic>CD86</italic> gene results in the alanine to threonine substitution, which further affects the antigen-presenting cells' signal transduction. Thus, the purpose of this study was to determine the association between CD86 +1057G/A polymorphism and the risk for chronic immune thrombocytopenia (cITP). The CD86 +1057G/A polymorphism in 158 cITP patients and 150 healthy controls were detected by polymerase chain reaction restriction fragment length polymorphism and then confirmed by DNA sequencing. In the patients with cITP, the frequencies of GG, AG and AA genotypes and G and A alleles were 18.4%, 58.8%, 22.8%, 47.8% and 52.2%, respectively. No difference in genotype and allele frequencies was detected in total cITP patients and normal controls (<italic>p</italic> = 0.913 and 0.845, respectively). Cases were subsequently classified by age at diagnosis, gender or clinical responses to glucocorticoids, and still no obvious discrepancy of genotype and allele frequencies was found between each of the groups and normal controls. In conclusion, this study suggests that CD86 +1057G/A polymorphism may be not associated with the genetic susceptibility to cITP in a Chinese population.</p> </abstract>