The lab studies the immunobiology of B-lymphocytes particularly the B cell survival factors BAFF and APRIL and their receptors BAFF-R, TACI and BCMA. Professor Mackay has shown that excess BAFF leads to autoimmunity in mice and is associated with human autoimmunity, in particular systemic lupus erythematosus (SLE). BAFF receptor TACI is highly expressed on memory B cells in SLE patients and BAFF-TACI interactions leads to heightened autoantibody production driving the disease pathology. Importantly, genetic deletion of TACI protects against SLE. However, the underlying mechanism remains largely unknown. In this project, we aim
This project will use a range of immunological techniques (mouse models of experimental SLE, flow cytometry, confocal microscopy, ELISA), metagenomic sequencing, microbiome analysis and metabolomics to characterise the immunological mechanisms of action. We will validate the research findings using clinical samples.
This project is suitable for a Master, Honour or PhD student.