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New mutations stabilize NOTCH1

Journal of Experimental Medicine
The Rockefeller University Press
Publication Date
DOI: 10.1084/jem.2048iti4
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  • Medicine


JEM_2048iti.indd IN THIS ISSUE | The Journal of Experimental Medicine 1733 Text by Hema Bashyam [email protected] All B cells need is BAFF 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. EBV covers its tracks Viruses that lie low inside cells after infection come under attack by the immune system when they reawaken and resume multiplying. Hislop et al. (page 1863) now reveal the mechanism used by the Epstein-Barr virus (EBV) to dodge host immunity during this reactivation phase. EBV initially infects and replicates within oral epithelial cells but later quietly hides out in B cells. During th

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