Immune thrombocytopenic purpura (ITP) is putatively associated with self-antibodies against platelet. FcgammaRIIb is a key regulator of B cell responses. To explore the relationship between the polymorphism of FcgammaRIIb 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 FcgammaRIIb 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 FcgammaRIIb 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. FcgammaRIIb transmembrane polymorphism had no relationship with chronic ITP or acute ITP when compared with healthy controls. The FcgammaRIIb 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 FcgammaRIIb transmembrane sequences was not associated with the development of ITP.