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Lupus-inducing B cells (arrows) develop even when T cells are missing (bottom).
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B cells usually conspire with T cells to break tolerance against the host and cause lupus. But Groom et al. (page 1959) now show that B cells don't always need T cells to egg them on. An activating cytokine empowers them to cause trouble all on their own.
This cytokine, called BAFF (B cell–activating factor), helps B cells survive as they transit through developmental checkpoints. BAFF also enhances T cell activation. With too much BAFF, however, even B cells that should have been eliminated—such as self-reactive ones—survive. The autoreactive antibodies first secreted by these cells are relatively harmless. But presumably with help from BAFF-activated T cells, these B cells switch their antibody genes and start producing pathogenic autoantibodies.
Groom et al. now find that the antibody-switching signal doesn't have to come from T cells. Mice that overexpressed BAFF but lacked T cells still developed lupus. The B cells instead derived the extra push through their Toll-like receptors (TLRs) 7 and 9, whose expression was strongly enhanced by BAFF. The authors speculate that nucleic acids released by dying cells might trigger these TLRs on self-reactive B cells.
The presence of disease-inducing antibodies even when T cells are absent might explain why not all lupus patients respond to treatments that suppress T cell functions. The team is now investigating whether these patients have high levels of BAFF. 
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