Project Summary
This project will continue the pioneering work linking defects in the nanoscale organization of the BCR to reduced BCR-mediated signal transduction, inefficient removal of cells expressing autoreactive BCRs and breaks in central tolerance. Briefly, B01 want to gain further insights into the mechanisms by which defective B cell activation leads to immunopathology. To this end, the molecular mechanism by which signals from the BCR are initiated will be study. Likewise, the role of the Cav1-FLNA axis in vivo will be investigated in the crosstalk between BCR and co-stimulatory signals provided by T cells.
