Postgraduate Profiles

Rhonda Taylor

Rhonda Taylor profile photo

Thesis: Transcriptional control of Complement Receptor 2 (CR2/CD21): Significance to B cell biology and autoimmunity

The ordered expression of surface receptors and transcription factors is tightly regulated during B cell development in order to maintain a functional B cell repertoire. Complement receptor 2 (CR2/CD21) is expressed on the surface of mature B cells but not pre-B or terminally differentiated plasma cells. It has been demonstrated that the correct level and timing of CR2 expression throughout B cell development is integral to optimal B cell function. Furthermore, CR2 is a candidate gene for the development of the autoimmune disease systemic lupus erythematosus, and altered transcriptional regulation of CR2 has been linked to an increased risk of developing autoimmune disease. The factors responsible for controlling the tightly regulated temporal expression pattern of CR2 remain to be defined. Furthermore, single nucleotide polymorphisms located in CR2 regulatory regions have previously been linked to an increased risk of developing the autoimmune disease systemic lupus erythematosus. Therefore, this project aims to further characterise the transcriptional regulation of human CR2 and the impact of single nucleotide polymorphisms on gene expression.

Why my research is important

This research will increase our current understanding of the transcriptional regulation of a gene intricately involved in the control of B cell function and development. Specifically, this project will characterise the transcriptional control of CR2 with the aim of identifying key transcription factors and global B cell regulators involved in controlling CR2 expression during B lineage commitment.

These studies are significant as altered transcriptional regulation of CR2 could contribute to the altered B cell function observed in autoimmune disease. Therefore, this research also aims to characterise the way in which regulatory single nucleotide polymorphisms may contribute to altered transcriptional regulation, aberrant B cell development and ultimately to autoimmune disease.