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Science 327 (5969): 1093-1094

Copyright © 2010 by the American Association for the Advancement of Science

Cell Biology

Turning Off Inflammation Signaling

Srividya Sriskantharajah, and Steven C. Ley

The name A20 may sound unassuming for a protein, but polymorphisms in the A20 gene locus have been identified as risk alleles for Crohn's disease, systemic lupus erythematosus, rheumatoid arthritis, type I diabetes, psoriasis, and atherosclerosis, suggesting important functions for A20 protein in autoimmunity. A20 is also a tumor suppressor for several types of B cell cancer, including Hodgkin's lymphoma and diffuse large B cell lymphoma (1). On page 1135 of this issue, Shembade et al. describe the means by which A20 acts through the transcription factor nuclear factor {kappa}B (NF-{kappa}B) to control inflammation (2).

Division of Immune Cell Biology, Medical Research Council, National Institute for Medical Research, London NW7 1AA, UK.

E-mail: sley{at}nimr.mrc.ac.uk


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Single-nucleotide Polymorphism and Haplotypes of TNIP1 Associated with Systemic Lupus Erythematosus in a Chinese Han Population.
D.-M. Zhang, L.-Q. Cheng, Z.-F. Zhai, L. Feng, B.-Y. Zhong, Y. You, N. Zhang, Z.-Q. Song, X.-C. Yang, F.-R. Chen, et al. (2013)
J Rheumatol 40, 1535-1544
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