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The role of cytokine mRNA stability in the pathogenesis of autoimmune disease

  1. Author:
    Seko, Y.
    Cole, S.
    Kasprzak, W.
    Shapiro, B. A.
    Ragheb, J. A.

  2. Author Address

    NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA. NCI, Basic Res Program, NIH, Frederick, MD 21701 USA. NCI, Canc Res Ctr, Nanobiol Program, NIH, Frederick, MD 21701 USA.;Ragheb, JA, NEI, Immunol Lab, NIH, Bldg 10,Rm 10N112,10 Ctr Dr MSC-1857, Bethesda, MD 20892 USA.;jr50b@nih.gov
    1. Year: 2006
    2. Date: May
  2. Journal: Autoimmunity Reviews
    1. 5
    2. 5
    3. Pages: 299-305
  4. Type of Article: Article
  5. ISSN: 1568-9972
  1. Abstract:

    Inflammatory cytokines such as interferon (IFN)-gamma, interleukin (IL)-2, tumor-necrosis factor (TNF)-alpha and IL-117 play an important role in the pathogenesis of cell-mediated autoimmune diseases. Cytokine gene expression is tightly regulated at the post-transcriptional level. Cytokine mRNA decay is dependent not only upon cis-elements in the RNA but also upon transacting factors such as the RNA binding proteins TTP, HuR, AUF-1, Nucleolin and YB-1. Physiologic signals,, for instance signaling through the CD28 receptor on T cells, can modulate the half-life of a select subset of cytokine mRNAs, such as IL-2. Distinct cis- and trans-acting elements in human and mouse IL-2 mRNA may account for the different pattern of CD28-mediated mRNA stabilization in these two species. TTP-deficient mice or mice with a deletion of the TNF-alpha mRNA ARE element develop a complex inflammatory syndrome that is associated with a prolonged TNF-alpha mRNA half-life and elevated levels of circulating TNF-alpha. This syndrome can be prevented by treatment with TNF-u blocking antibodies. Evidence from mice with altered cytokine mRNA stability, along with human data, suggests that imbalance between the stability and decay of inflammatory cytokine mRNAs could represent a basic mechanism leading to autoimmunity. Published by Elsevier B.V.

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External Sources

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  2. DOI: 10.1016/j.autrev.2005.10.013
  3. View record in Web of Science®
  4. WOS: 000238925700001

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