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Life Sci Alliance. 2019 May 16;2(3). pii: e201800244. doi: 10.26508/lsa.201800244. Print 2019 Jun.

MicroRNA-155 is essential for the optimal proliferation and survival of plasmablast B cells.

Author information

1
Lymphocyte Signalling and Development, Babraham Institute, Cambridge, UK.
2
Bioinformatics, Babraham Institute, Cambridge, UK.
3
Lymphocyte Signalling and Development, Babraham Institute, Cambridge, UK R.Leyland@shu.ac.uk.
4
Biomolecular Sciences Research Centre, Sheffield Hallam University, Sheffield, UK.

Abstract

A fast antibody response can be critical to contain rapidly dividing pathogens. This can be achieved by the expansion of antigen-specific B cells in response to T-cell help followed by differentiation into plasmablasts. MicroRNA-155 (miR-155) is required for optimal T-cell-dependent extrafollicular responses via regulation of PU.1, although the cellular processes underlying this defect are largely unknown. Here, we show that miR-155 regulates the early expansion of B-blasts and later on the survival and proliferation of plasmablasts in a B-cell-intrinsic manner, by tracking antigen-specific B cells in vivo since the onset of antigen stimulation. In agreement, comparative analysis of the transcriptome of miR-155-sufficient and miR-155-deficient plasmablasts at the peak of the response showed that the main processes regulated by miR-155 were DNA metabolic process, DNA replication, and cell cycle. Thus, miR-155 controls the extent of the extrafollicular response by regulating the survival and proliferation of B-blasts, plasmablasts and, consequently, antibody production.

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