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Let-7 Suppresses B Cell Activation through Restricting the Availability of Necessary Nutrients

Shuai Jiang1, Wei Yan2, Shizhen Emily Wang2

  • 1Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA 91125, USA.

Cell Metabolism
|January 17, 2018
PubMed

Insights

The let-7 microRNA cluster (let-7adf) acts as a metabolic brake, inhibiting B cell antibody production by controlling glucose and glutamine uptake. This finding reveals a novel regulatory mechanism in B cell activation.

Area of Science:

  • Immunology
  • Molecular Biology
  • Metabolism

Background:

  • B cell activation requires precise control of nutrient uptake and utilization, particularly glucose and glutamine.
  • MicroRNAs of the let-7 family are known regulators of metabolic processes.

Purpose of the Study:

  • To investigate the role of the let-7a-1/let-7d/let-7f-1 cluster (let-7adf) in B cell activation and antibody production.
  • To elucidate the molecular mechanisms by which let-7adf influences B cell metabolism and function.

Main Methods:

  • Utilized engineered mouse models with B cell-specific overexpression or knockout of let-7adf.
  • Analyzed T cell-independent (TI) antigen-induced immunoglobulin (Ig)M antibody production.
  • Investigated nutrient uptake, utilization, and key metabolic gene expression (Hk2, Slc1a5, Gls) regulated by c-Myc.

Main Results:

  • let-7adf specifically inhibits TI antigen-induced IgM antibody production.
  • Altered let-7adf levels (overexpression or deletion) lead to changes in TI-IgM production.
  • let-7adf suppresses glucose and glutamine acquisition and utilization by targeting Hk2, Slc1a5, and Gls via c-Myc regulation.

Conclusions:

  • let-7adf functions as a novel "metabolic brake" on B cell antibody production.
  • let-7adf regulates B cell metabolism by controlling key nutrient transporters and metabolic enzymes.
  • This study uncovers a critical link between microRNA-mediated metabolic control and adaptive immunity.
Keywords:
B cellsantibody productionglutamine metabolismglycolysislet-7

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