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Published on: October 14, 2016
miR-148a controls metabolic programming and survival of mature CD19-negative plasma cells in mice
Katharina Pracht1, Julia Meinzinger1, Sebastian R Schulz1
1Division of Molecular Immunology, Internal Medicine III, University Hospital Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.
Abstract:
Long-lived antibody-secreting plasma cells are essential to establish humoral memory against pathogens. While a regulatory transcription factor network has been established in plasma cell differentiation, the regulatory role of miRNAs remains enigmatic. We have recently identified miR-148a as the most abundant miRNA in primary mouse and human plasma cells. To determine whether this plasma cell signature miRNA controls the in vivo development of B cells into long-lived plasma cells, we established mice with genomic, conditional, and inducible deletions of miR-148a. The analysis of miR-148a-deficient mice revealed reduced serum Ig, decreased numbers of newly formed plasmablasts and reduced CD19-negative, CD93-positive long-lived plasma cells. Transcriptome and metabolic analysis revealed an impaired glucose uptake, a reduced oxidative phosphorylation-based energy metabolism, and an altered abundance of homing receptors CXCR3 (increase) and CXCR4 (reduction) in miR-148a-deficient plasma cells. These findings support the role of miR-148a as a positive regulator of the maintenance of long-lived plasma cells.
Insights
MicroRNAs, specifically miR-148a, are crucial for maintaining long-lived plasma cells, which are vital for humoral immunity. Loss of miR-148a impairs B cell development and reduces antibody production.
Area of Science:
- Immunology
- Molecular Biology
- Genetics
Background:
- Long-lived plasma cells are essential for establishing humoral immune memory against pathogens.
- While transcription factors regulating plasma cell differentiation are known, the role of microRNAs (miRNAs) is unclear.
- miR-148a is identified as the most abundant miRNA in primary mouse and human plasma cells.
Purpose of the Study:
- To investigate the role of miR-148a in the in vivo development and maintenance of long-lived plasma cells.
- To determine if miR-148a regulates B cell differentiation into antibody-secreting plasma cells.
Main Methods:
- Generation of mice with conditional and inducible deletions of miR-148a.
- Analysis of serum immunoglobulin (Ig) levels and plasma cell populations (plasmablasts, long-lived plasma cells).
- Transcriptome and metabolic analyses of miR-148a-deficient plasma cells, including glucose uptake and oxidative phosphorylation.
Main Results:
- miR-148a-deficient mice exhibited reduced serum Ig and fewer plasmablasts and long-lived plasma cells.
- Deficiency in miR-148a led to impaired glucose uptake and reduced oxidative phosphorylation-based energy metabolism.
- Altered expression of homing receptors CXCR3 (increased) and CXCR4 (decreased) was observed in miR-148a-deficient plasma cells.
Conclusions:
- miR-148a acts as a positive regulator in the maintenance of long-lived plasma cells.
- This miRNA influences B cell development, energy metabolism, and homing receptor expression in plasma cells.
- miR-148a is a key component of the regulatory network governing humoral immunity.
