Journal of Leukocyte Biology BioLegend: Treg, Th17, Stem Cell
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Originally published online as doi:10.1189/jlb.1103536 on April 1, 2004

Published online before print April 1, 2004
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(Journal of Leukocyte Biology. 2004;76:42-47.)
© 2004 by Society for Leukocyte Biology

Post-transcriptional regulation of proinflammatory proteins

Paul Anderson1, Kristine Phillips, Georg Stoecklin and Nancy Kedersha

Division of Rheumatology, Immunology and Allergy, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts

1Correspondence: Division of Rheumatology, Immunology and Allergy, Brigham and Women’s Hospital, Smith 652, One Jimmy Fund Way, Boston, MA 02115. E-mail: panderson{at}rics.bwh.harvard.edu

Post-transcriptional mechanisms play a critical role in regulating the expression of numerous proteins that promote inflammatory arthritis. The mRNAs encoding a subset of these proteins possess adenine/uridine-rich elements (AREs) in their 3'-untranslated regions that profoundly influence the rate at which mRNA is degraded and translated into protein. Tristetraprolin (TTP) and T cell intracellular antigen-1 (TIA-1) are ARE-binding proteins that dampen the expression of this class of proteins by promoting mRNA degradation and protein translation, respectively. We have discovered that TIA-1 and TTP function as arthritis-suppressor genes: TIA-1–/– mice develop mild arthritis, TTP–/– mice develop severe arthritis, and TIA-1–/–TTP–/– mice develop very severe arthritis. Paradoxically, lipopolysaccharide (LPS)-activated macrophages derived from TIA-1–/–TTP–/– macrophages produce less tumor necrosis factor {alpha} (TNF-{alpha}) than TIA-1–/– or TTP–/– macrophages. The bone marrows of these mice exhibit increased cellularity, reflecting the presence of mature neutrophils that secrete TNF-{alpha} in response to LPS stimulation. We hypothesize that TIA-1–/–TTP–/– neutrophils are a source of arthritigenic TNF-{alpha}, which promotes severe erosive arthritis in these mice.

Key Words: tristetraprolin • T cell intracellular antigen-1 • adenine/uridine-rich elements




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