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(Journal of Leukocyte Biology. 2002;72:410-416.)
© 2002 by Society for Leukocyte Biology

Identification of downstream genes up-regulated by the tumor necrosis factor family member TALL-1

Liang-Guo Xu*, Min Wu*,{dagger}, Jiancheng Hu*, Zhonghe Zhai{dagger} and Hong-Bing Shu*,{dagger}

* Department of Immunology, National Jewish Medical and Research Center, University of Colorado Health Sciences Center, Denver; and
{dagger} Department of Cell Biology and Genetics, College of Life Sciences, Peking University, Beijing, China

Correspondence: Dr. Hong-Bing Shu, Department of Immunology, National Jewish Medical and Research Center, 1400 Jackson Street, K516c, Denver, CO 80206. E-mail: shuh{at}njc.org

TALL-1 is a member of the tumor necrosis factor family that binds to BCMA, TACI, and BAFF-R, three receptors mostly expressed by mature B lymphocytes. Previous studies have shown that the TALL-1 signaling is critically involved in B cell proliferation, maturation, and progression of lupus-like, autoimmune diseases. In this report, we performed cDNA subtractive hybridization experiments to identify downstream genes up-regulated by TALL-1. These experiments indicated that 10 genes, including interleukin (IL)-10, lymphocyte activation gene-1 (LAG-1), GCP-2, PBEF, ferritin, PIM-2, TFG, CD27 ligand, DUSP5, and archain, were up-regulated at the mRNA level by TALL-1 stimulation in B lymphoma RPMI-8226 cells and/or primary B lymphocytes. We also demonstrated that TALL-1 activated transcription of IL-10 and LAG-1 in a nuclear factor-{kappa}B-dependent manner in reporter gene assays. Moreover, our findings indicated BAFF-R, but not TACI, could dramatically up-regulate IL-10 secretion by RPMI-8226 cells. The identification of TALL-1-up-regulated genes will help explain the mechanisms of TALL-1-triggered biological and pathological effects and to identify molecular targets for intervention of lupus-like autoimmune diseases.

Key Words: B lymphocytes • autoimmunity • IL-10 • gene regulation




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