An FcγRIIb transmembrane polymorphism in Chinese ITP patients

Abstract

Immune thrombocytopenic purpura (ITP) is putatively associated with self-antibodies against platelet. FcγRIIb is a key regulator of B cell responses. To explore the relationship between the polymorphism of FcγRIIb transmembrane portion and ITP, a cohort control study was carried out. Two hundred and eighty ITP patients and 243 healthy volunteers were enrolled in this study. Most of the ITP patients were followed up for at least 6 months following diagnosis to allow classification of chronic or acute ITP. The concentrations of IgG/IgA/IgM antiplatelet antibodies (PAIgG/IgA/IgM) were determined by a competitive micro-ELISA method. Genomic DNA was isolated and a single nucleotide polymorphism (SNP) of the FcγRIIb transmembrane exon located at position 695 was detected by real-time florescent PCR. The presence of 695T > C polymorphism was detected by the pattern of melting curve peak. The distribution of FcγRIIb genotypes was not significantly different between ITP patients and healthy controls. The homozygous 695C/C proportion in child-onset ITP patients was lower than that in the healthy control group, but had no statistical significance. FcγRIIb transmembrane polymorphism had no relationship with chronic ITP or acute ITP when compared with healthy controls. The FcγRIIb 695C allele carrying had no influence on the levels of platelet antibodies such as IgG, IgA or IgM. However, the PAIgA/IgM levels associated with the clinical experience of developing chronic ITP. Here we concluded one hot-spot polymorphism in FcγRIIb transmembrane sequences was not associated with the development of ITP.

• Immune thrombocytopenic purpura, FcγRIIb, single nucleotide polymorphism, platelet associated immunoglobulin