Dr. Natalia Giltiay studies the role of B cell in immunopathology of autoimmune diseases. A hallmark of SLE, SjS, and other autoimmune diseases is the production of auto-antibodies (auto-Abs), directed against ubiquitous cellular components, such as DNA, RNA, and other nuclear antigens. Genetic data have supported a strong link between genetic variations of TLR7 and SLE susceptibility. Still, very little has been done to define how dysregulation of TLR7 expression might affect human B cells and contribute to the development of SLE. Current projects in the lab are focused on identifying new signaling mechanisms involved in the regulation of TLR7 expression, specifically in B cells. We are also exploring the effects of TLR7 over-expression in different B cell subsets in human and mice with respect to cell activation, auto-Ab production and cytokine production. We are currently testing how genetic variations of TLR7 affect B cells in SLE patients.
In collaboration with Dr. Clark’s Lab, we are also studying the effects of Epratuzumab (Emab), a humanized anti-CD22 mAb currently in clinical trials for treatment of SLE, on B cell responses, in an effort to explain how Emab might function to suppress B cell activation in SLE.
Other areas of research have been focused on the role of plasmacytoid DCs (pDCs) in regulating T- and B- cell responses and how antigen-targeting to pDCs via pDC-specific C-type lectin receptor BDCA2, can be used to promote immune tolerance.