Tristetraprolin as a Therapeutic Target in Inflammatory Disease

Trends Pharmacol Sci. 2016 Oct;37(10):811-821. doi: 10.1016/ Epub 2016 Aug 5.


Members of the tristetraprolin (TTP) family of RNA-binding proteins are found in all major eukaryotic groups. TTP family members, from plants through humans, can bind adenosine-uridine rich elements in target mRNAs with high affinity. In mammalian cells, these proteins then promote deadenylation and decay of target transcripts. Four such proteins are found in mice, of which the best studied is TTP. When the gene encoding TTP is disrupted in mice, the animals develop a severe syndrome of arthritis, autoimmunity, cachexia, dermatitis, and myeloid hyperplasia. Conversely, recent overexpression studies have demonstrated protection against several experimental models of immune inflammatory disease. This endogenous anti-inflammatory protein could serve as the basis for novel approaches to therapy of similar conditions in humans.

Keywords: autoimmunity; deadenylation; inflammation; mRNA decay; tumor necrosis factor.

Publication types

  • Review
  • Research Support, N.I.H., Intramural

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Autoimmune Diseases / drug therapy
  • Autoimmune Diseases / genetics
  • Autoimmune Diseases / immunology
  • Disease Models, Animal
  • Drug Design
  • Humans
  • Inflammation / drug therapy*
  • Inflammation / genetics
  • Inflammation / immunology
  • Mice
  • RNA, Messenger / metabolism
  • Tristetraprolin / genetics*


  • Anti-Inflammatory Agents
  • RNA, Messenger
  • Tristetraprolin