Systemic lupus erythematosus (SLE or lupus) is a chronic autoimmune disease in which the immune system attacks the body?s cells and tissues.
Although B cells are known to play a role in this disease, the exact way in which their function is disrupted remains poorly understood.
In a study appearing online on July 19 in advance of publication in the August print issue of the Journal of Clinical Investigation, Chandra Mohan and colleagues from UT Southwestern Medical Center examined different strains of lupus-prone mice in order to address this question.
They report that different signaling pathways are upregulated in lupus B cells as the disease evolves. However, the very same pathways are shown to be upregulated in B cells from mice with different lupus-prone genetic backgrounds, indicating that although the genetic trigger of the disease may differ, these different triggers ultimately converge upon a shared set of signaling pathways to induce disease. Finally, the authors were able to treat lupus in these animals using a derivative of the drug rapamycin, thereby identifying one of these pathways (involving the molecules known as AKT and mTOR) as being an attractive therapeutic target in lupus.
TITLE: Shared signaling networks active in B cells isolated from genetically distinct mouse models of lupus