Alternative splicing directs two IL-20R2 isoforms and is responsible for the incomplete gene knockout via the exon I ablation

Genes Immun. 2016 Jun;17(4):220-7. doi: 10.1038/gene.2016.13. Epub 2016 Mar 24.

Abstract

Two heterodimeric receptors consisting of interleukin (IL)-20R2 are shared by three of the IL-20 family of cytokines, IL-19, IL-20 and IL-24. Along with IL-22, these cytokines are downstream effectors of IL-23 and have been implicated in keratinocyte functions and the pathogenesis of psoriasis. Surprisingly, whereas knocking out either the IL-23 or IL-22 gene abolished imiquimod-induced psoriatic phenotypes in mice, similar attempt for IL-20R2 had little effect. Here, we report that the apparent disparity may result from a new IL-20R2 isoform encoded by an alternatively spliced transcript which survived the previous attempt for IL-20R2 gene knockout via the exon I deletion.

MeSH terms

  • Alternative Splicing*
  • Animals
  • Exons
  • Gene Deletion
  • Interleukin-23 / genetics
  • Interleukin-23 / metabolism
  • Interleukins / genetics
  • Interleukins / metabolism
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Protein Isoforms / genetics
  • Protein Isoforms / metabolism
  • Receptors, Interleukin / genetics*
  • Receptors, Interleukin / metabolism

Substances

  • Interleukin-23
  • Interleukins
  • Protein Isoforms
  • Receptors, Interleukin
  • interleukin-20 receptor
  • interleukin-22