Interleukin 9 prevents immune thrombocytopenia in mice via JAK/STAT5 signaling

Exp Cell Res. 2020 Mar 1;388(1):111801. doi: 10.1016/j.yexcr.2019.111801. Epub 2019 Dec 23.


Immune thrombocytopenia (ITP) is an autoimmune disorder characterized by autoimmune-mediated platelet destruction and impaired platelet production, which can lead to an increased risk of bleeding. The clinical management of ITP currently remains a challenge for hematologists. We explored the role of interleukin-9 (IL-9) in the treatment of CD41-induced ITP, and investigated its underlying mechanisms in a CD41-induced ITP mouse model. IL-9 treatment increased the numbers of mature megakaryocytes (CD41+CD42d+) and CD41+Sca-1+ cells in the bone marrow in these model mice, while IL-9 receptor (IL-9R) small interfering RNA (siRNA) inhibited the process. Moreover, phosphorylated signal transducer and activator of transcription 5 (STAT5), as a downstream molecule of IL-9R, was increased after IL-9 treatment. We next investigated the source of IL-9 in bone marrow, osteoblasts produced the highest level of IL-9. These results confirmed that IL-9 could prevent CD41-induced ITP in BALB/c mice by regulating osteoblasts and activating IL-9R/STAT5 signaling in megakaryocytes, thus providing further evidence for IL-9 as a promising therapeutic agent for the treatment of ITP.

Keywords: Immune thrombocytopenia; Interleukin 9; STAT5.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cells, Cultured
  • Interleukin-9 / pharmacology
  • Interleukin-9 / therapeutic use*
  • Janus Kinases / metabolism*
  • Male
  • Megakaryocytes / drug effects
  • Megakaryocytes / metabolism
  • Mice
  • Mice, Inbred BALB C
  • Osteoblasts / drug effects
  • Osteoblasts / metabolism
  • Purpura, Thrombocytopenic, Idiopathic / drug therapy*
  • Purpura, Thrombocytopenic, Idiopathic / prevention & control
  • Receptors, Interleukin-9 / metabolism
  • STAT5 Transcription Factor / metabolism*
  • Signal Transduction*


  • Interleukin-9
  • Receptors, Interleukin-9
  • STAT5 Transcription Factor
  • Janus Kinases