A new model to study BAFF-independent SLE

In a new experimental model of systemic lupus erythematosus (SLE), lupus-prone mice with genetic deficiency of B cell activating factor (BAFF) can still develop full-blown disease. The NZM.Baff^–/– mice express a human BCL2 transgene (Tg) in their B cells, thus preserving B cell survival largely independent of BAFF-triggered signals. In NZM.Baff^–/–BCL2^Tg mice, immunological, serological and clinical features of SLE developed more rapidly than in NZM wild-type mice. This model could help explain why some patients with SLE fail to respond to anti-BAFF therapy.