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MicroRNA-146a-deficient mice develop immune complex glomerulonephritis.

Lucile Amrouche1,2,3, Sylvaine You4,5, Virginia Sauvaget6

  • 1INSERM, U1151, Paris, France. lucile.amrouche@aphp.fr.

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|November 1, 2019
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Summary

MicroRNA-146a deficiency in mice leads to age-dependent autoimmunity and immune complex glomerulonephritis. This occurs due to altered B cell responses and reduced Kim1/Tim1 expression, highlighting miR-146a's role in kidney immune regulation.

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Area of Science:

  • Nephrology
  • Immunology
  • Molecular Biology

Background:

  • MicroRNAs (miRNAs) are crucial in kidney function and disease.
  • The specific role of miR-146a in immune glomerulonephritis remains largely unknown.
  • miR-146a is implicated in innate immunity and kidney tubular cell injury responses.

Purpose of the Study:

  • To investigate the role of miR-146a in the development of autoimmune glomerulonephritis.
  • To examine the impact of miR-146a deficiency on renal and immune cell phenotypes.
  • To elucidate the mechanisms linking miR-146a, B cell homeostasis, and kidney inflammation.

Main Methods:

  • Comparative analysis of miR-146a knockout (miR-146a-/-) and wild-type (miR-146a+/+) mice at 12 months of age.
  • Assessment of renal and immune phenotypes, including autoantibody production and glomerulonephritis.
  • Evaluation of transmembrane protein Kim1/Tim1 expression, B cell subsets (regulatory B cells, memory B cells, plasmablasts), and IL-10 production.

Main Results:

  • miR-146a-/- mice developed age-dependent autoimmunity, characterized by anti-dsDNA antibodies and immune complex glomerulonephritis.
  • Reduced Kim1/Tim1 expression was observed in the kidneys and immune cells of miR-146a-/- mice.
  • An increase in memory B cells and plasmablasts, alongside a decrease in regulatory B cells with impaired IL-10 production, was noted in miR-146a-/- mice.

Conclusions:

  • miR-146a deficiency promotes an autoimmune syndrome with immune complex glomerulonephritis in aging mice.
  • Altered B cell responses, potentially linked to Kim1/Tim1 deficiency, contribute to glomerulonephritis pathogenesis.
  • This study establishes a significant role for miR-146a in the development of immune-mediated glomerulonephritis.