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Ann Rheum Dis 72:ii90-ii95 doi:10.1136/annrheumdis-2012-202203
  • Papers
  • Supplement

MicroRNA-146a in autoimmunity and innate immune responses

  1. Minoru Satoh3,4
  1. 1Department of Oral Biology, University of Florida, Gainesville, Florida, USA
  2. 2Department of Anatomy and Cell Biology, University of Florida, Gainesville, Florida, USA
  3. 3Division of Rheumatology and Clinical Immunology, Department of Medicine, University of Florida, Gainesville, Florida, USA
  4. 4Department of Pathology, Immunology and Laboratory Medicine, University of Florida, Gainesville, Florida, USA
  1. Correspondence to Professor Edward K L Chan, Department of Oral Biology, University of Florida, Gainesville, FL 32610-0424, USA; echan{at}ufl.edu
  • Accepted 7 August 2012
  • Published Online First 19 December 2012

Abstract

MicroRNA (miRNA) are approximately 22 nucleotide single-stranded RNA that regulate the stability of target messenger RNA by selective binding to specific sites at the 3′-untranslated regions (UTR). This triggers repression in translation and mRNA degradation. It has been estimated that approximately 60% of all mRNA are under the control of miRNA. Among the known hundreds of miRNA, some are considered master regulators controlling either a single or multiple cellular pathways. Some miRNA are known to affect development and cell differentiation, while others are implicated in immunity and autoimmune diseases. A very interesting example is miR-146a, which has been reported to be downregulated in systemic lupus erythematosus and upregulated in rheumatoid arthritis (RA). Several groups have recently focused their attention on miRNA in the pathogenesis of RA. Interestingly, the expression of miR-146a is upregulated in different cell types and tissues in RA patients. miRNA in RA could also be considered as possible future targets for new therapeutic approaches. This discussion will focus on the current understanding in the function of miR-146a in endotoxin tolerance and cross-tolerance, and how it may contribute to modulate the overproduction of known pathogenic cytokines, such as tumour necrosis factor α.