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Science 16 June 2006:
Vol. 312. no. 5780, p. 1569
DOI: 10.1126/science.312.5780.1569o
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This Week in Science
Systemic lupus erythematosus (SLE) is an autoimmune disease in which B cells produce antibodies directed against self components of the cell, in particular, nucleic acids and their associated proteins. Two studies offer clues to genes that may influence B cell responses and susceptibility to SLE (see the Perspective by Goodnow). Pisitkun et al. (p. 1669, published online 18 May) studied a genetically well-defined mouse model for SLE, in which a male-specific increase in the severity of disease is associated with the duplication of a particular X-chromosomal segment on the Y chromosome, termed the Y-linked autoimmune accelerator (Yaa). In bone-marrow mixing experiments, the auto-antibodies generated by Yaa-positive cells were specific for RNA-related nucleolar antigens. These antigens also act as ligands for Toll-like receptors (TLRs), including TLR7, and further genetic characterization revealed that the duplication of the TLR7 gene by the Yaa region made the B cells in these mice more sensitive to TLR7 activation. Kumar et al. (p. 1665), who also used a mouse SLE model, observed that a particular allelic form of the signaling protein encoded by Ly108 made B cells proliferate rather than die in response to signals that would normally maintain B cell tolerance, and allowed the B cells to make self-reactive antibodies.
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