I am a Rheumatologist with clinical experience and experience in clinical research. I have a Master’s Degree focused on study design and analysis, and a Ph.D. on Molecular Medicine. During the last five years, I have been studying the role of B cells in patients with Systemic Lupus Erythematosus, designing and performing experiments to study B cell biology. I have published on B cell tolerance in SLE and described a phenotype of antigen experienced autoreactive B cells in patients with SLE.
My overall research goal is to understand the role of intrinsic and extrinsic B cells abnormalities in SLE, trying to develop precision therapeutics to improve the prognosis of SLE.
Antibodies are proteins that normally have protective functions. They are made by plasma cells, cells, which are derived from B cells. Systemic lupus erythematosus (SLE) is characterized by the presence of pathogenic autoantibodies, antibodies made against substances formed by a person’s own body, specifically against components present in the nucleus of a cell (antinuclear antigens or ANA). These autoantibodies cause damage in tissues and contribute to inflammation. In healthy people, there are circulating B cells that are able to produce autoantibodies against ANA (ANA+ B cells), however, there are checkpoints that prevent them from differentiating into plasma cells. It is not known if these ANA+ B cells are more prone to differentiate into plasma cells in patients with SLE or if the antibodies that they produce are different compared to those made by ANA+ B cells from healthy people. The scientific objective of this proposal is to characterize ANA+ B cells, their response to stimulus and their differentiation to plasma cells in SLE patients, those with active disease, and those with a quiescent disease (in remission), and in healthy controls, and to understand their spectrum of antigens recognized. These studies will inform us about regulation of autoimmunity in patients with SLE, and if mechanisms that control ANA+ B cells are relevant to achieve remission in SLE. This information can be relevant for the development of precision therapy focused on ANA+ B cells for patients with SLE.