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Interleukin-10 control of pre-miR155 maturation involves CELF2

Jeff S J Yoon1,2,3, Mike K Wu1,2,3, Tian Hao Zhu3

  • 1Immunity and Infection Research Centre, Vancouver Coastal Health Research Institute, Vancouver, Canada.

Plos One
|April 24, 2020
PubMed

Insights

Interleukin-10 (IL10) reduces inflammation by inhibiting microRNA-155 (miR155) maturation. This involves the RNA binding protein CELF2, which is crucial for IL10

Area of Science:

  • Immunology
  • Molecular Biology
  • Gene Regulation

Background:

  • Interleukin-10 (IL10) is a key anti-inflammatory cytokine.
  • IL10 suppresses pro-inflammatory responses, including microRNA-155 (miR155) expression in macrophages.
  • miR155 promotes inflammation by upregulating TNFα and downregulating SHIP1 and SOCS1.

Purpose of the Study:

  • To elucidate the mechanism by which IL10 inhibits pre-miR155 maturation.
  • To identify proteins interacting with pre-miR155 upon IL10 stimulation in macrophages.

Main Methods:

  • Macrophage culture and stimulation with lipopolysaccharide (LPS) and IL10.
  • Isolation of proteins associated with pre-miR155.
  • CRISPR-Cas9 mediated knockdown of candidate proteins.
  • Quantitative assessment of miR155, TNFα, SHIP1, and SOCS1 expression.

Main Results:

  • CELF2 (CUGBP, ELAV-Like Family member 2) was identified as a protein associating with pre-miR155 in IL10-treated macrophages.
  • IL10 treatment increased the association of CELF2 with pre-miR155.
  • Knockdown of CELF2 using CRISPR-Cas9 abolished IL10's inhibitory effect on miR155 and TNFα expression.

Conclusions:

  • CELF2 is a critical mediator of IL10's anti-inflammatory function.
  • IL10 utilizes CELF2 to interfere with pre-miR155 maturation, thereby suppressing pro-inflammatory cytokine production.
  • Targeting the IL10-CELF2-miR155 axis may offer therapeutic strategies for inflammatory diseases.

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