Abstract
Systemic Lupus Erythematosis (SLE) is a common autoimmune disease affecting mainly women and people of non Caucasian descent. This disease varies in severity and presentation but death due to renal failure is the most common outcome. The BXSB Yaa mouse has been a widely accepted model for the study of SLE. In an attempt to further illuminate the pathogenesis of this disease, CD8 and interleukin 15 were genetically removed from this model. The resulting congenic mouse develops an SLE like disease at an accelerated rate, succumbing to disease in half the time of the BXSB Yaa (3 months versus 6 months of age). Immunoglobulin levels are high at an early age in these mice. A loss of architecture and overwhelming plasmablast cell populations are seen histologically in the spleen and lymph nodes. These plasmablast cells were also found in the gastric mucosa, lung parenchyma, and renal tissues. Through immunoflorescence (IFA) and flow cytometry of splenic tissue, a number of these cells appear to be B220 negative and CD138 positive. There also appears to be an association with CD5, CD49b, and CD43. IFA has also revealed a loss of normal orientation between B220 labeled and CD4 labeled cells in the spleen and lymph nodes of these mice as well as many CD138 positive cells throughout these tissues. Further characterization of these cells is being pursued as well as age related studies in these mice to further define the pathogenesis of SLE.
