Loss of miR-182 affects B-cell extrafollicular antibody response

Immunology. 2016 Jun;148(2):140-9. doi: 10.1111/imm.12592. Epub 2016 Mar 8.

Abstract

MicroRNAs have been shown to play a role in B-cell differentiation and activation. Here, we found miR-182 to be highly induced in activated B cells. However, mice lacking miR-182 have normal B-cell and T-cell development. Interestingly, mutant mice exhibited a defective antibody response at early time-points in the immunization regimen when challenged with a T-cell-dependent antigen. Germinal centres were formed but the generation of extrafollicular plasma cells was defective in the spleens of immunized miR-182-deficient mice. Mutant mice were also not able to respond to a T-cell-independent type 2 antigen, which typically elicited an extrafollicular B-cell response. Taken together, the data indicated that miR-182 plays a critical role in driving extrafollicular B-cell antibody responses.

Keywords: antibody response; extrafollicular B cells; germinal centres; miR-182.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibody Formation / genetics
  • B-Lymphocytes / physiology*
  • Cell Differentiation / genetics
  • Cells, Cultured
  • Germinal Center / physiology*
  • Immunization
  • Lymphocyte Activation / genetics
  • Mice
  • Mice, 129 Strain
  • Mice, Inbred C57BL
  • Mice, Knockout
  • MicroRNAs / genetics*
  • Plasma Cells / physiology*
  • T-Lymphocytes / immunology*

Substances

  • MicroRNAs
  • Mirn182 microRNA, mouse