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• W2001033766 abstract "Abstract Rationale A coding region single nucleotide polymorphism of CD23, C371T, has been identified and associated with enhanced T cell responses to antigen in allergic subjects. The mechanisms involved in this process are still unknown. Methods In this study, we have been able to clone CD23a cDNA in plasmid pCMVScript-CD23a-C with the C allele at position 371. Site directed mutagenesis was performed to produce a mutant pCMVScript-CD23a-T with a T instead of C allele at 371. Results After transfection of pCMVScript-CD23a-C only (CC), mixture of pCMVScript-CD23a-T and pCMVSCript-CD23a-C (CT), and pCMVScript-CD23a-T only (TT) into Cos-7 cells, no differences in expression levels were observed among these transfected groups in terms of CD23 expression on Cos-7 cell membrane and mRNA level. However, sCD23 in culture media was undetectable for TT while detectable sCD23 was found for CC than CT after 48 hrs of transfection. Treatment of transfected cells with proteases such as Human Leukocyte Elastase (HLE), Cathepsin G and the allergen Der p I resulted in lower level of CD23 on cell membrane in CC and CT transfected cells compared to TT cells. Conclusions These results indicate that mutation of C371T in CD23 caused the resistance of membrane CD23 to endogenous and added protease catalyzed cleavage, suggesting that the change in biological function for CD23 after mutation might be due to the resistance of the TT variant to cleavage and turnover. This then might explain enhanced antigen presentation of IgE-antigen complex via a receptor that is more resistant to turnover." @default.
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• W2001033766 date "2004-02-01" @default.
• W2001033766 modified "2023-09-27" @default.
• W2001033766 title "Polymorphism C371T results in resistance of CD23 to enzymatic cleavage in cultured cells*1" @default.
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• W2001033766 doi "https://doi.org/10.1016/j.jaci.2004.01.679" @default.
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