CD19 Hyperexpression Augments Sle1-Induced Humoral Autoimmunity but Not Clinical Nephritis.

The article presents a study which investigated the degree to which generalized B cell hyperactivity can amplify lupus pathogenesis. The authors suggest that generalized B cell hyperactivity may augment humoral autoimmunity, but may not suffice to engender end-organ disease in lupus. They also point to the presence of an additional distal checkpoint that dissociates pathogenic autoantibody formation and renal immunoglobulin deposition from the progression to clinical nephritis in lupus.