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MicroRNA-155 is essential for the optimal proliferation and survival of plasmablast B cells
Giuseppina Arbore1, Tom Henley1, Laura Biggins2
1Lymphocyte Signalling and Development, Babraham Institute, Cambridge, 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.
Insights
MicroRNA-155 (miR-155) is crucial for B-cell expansion and survival, impacting antibody production during T-cell-dependent immune responses. This study reveals miR-155 controls B-blast expansion and plasmablast proliferation for effective pathogen containment.
Area of Science:
- Immunology
- Molecular Biology
- Cell Biology
Background:
- Rapid antibody responses are vital for controlling fast-growing pathogens.
- T-cell help drives antigen-specific B cell expansion and differentiation into plasmablasts.
- MicroRNA-155 (miR-155) is known to be essential for T-cell-dependent extrafollicular responses, but the underlying cellular mechanisms are unclear.
Purpose of the Study:
- To elucidate the cellular processes regulated by microRNA-155 (miR-155) in B cells during T-cell-dependent immune responses.
- To investigate the role of miR-155 in the early expansion of B-blasts and the subsequent survival and proliferation of plasmablasts.
Main Methods:
- In vivo tracking of antigen-specific B cells from the onset of antigen stimulation.
- Comparative transcriptome analysis of miR-155-sufficient and miR-155-deficient plasmablasts at the peak of the immune response.
Main Results:
- miR-155 intrinsically regulates the early expansion of B-blasts.
- miR-155 controls the survival and proliferation of plasmablasts.
- Transcriptome analysis indicated miR-155 primarily regulates DNA metabolic processes, DNA replication, and the cell cycle in plasmablasts.
Conclusions:
- MicroRNA-155 (miR-155) is a key regulator of B-cell proliferation and survival during extrafollicular responses.
- miR-155 controls the magnitude of the extrafollicular response by influencing B-blast and plasmablast dynamics.
- These findings highlight miR-155's critical role in antibody production and host defense against pathogens.
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