HnRNPK restrains memory precursor and plasma cell differentiation to control germinal center B-cell output.

HnRNPK limits memory B-cell and plasma cell differentiation, maintaining germinal center B-cell output by regulating transcription and metabolism.

• Why it matters: Understanding how B-cell fate decisions are controlled is crucial for improving immune responses and vaccine design, yet the transcriptional and metabolic mechanisms remain unclear.
• What they did: Researchers created mice with B-cell-specific knockout of hnRNPK, revealing that its absence increases plasma cell differentiation and reduces germinal center B-cell numbers through altered gene expression and glycolytic activity.
• The result: HnRNPK suppresses MB cell factors Hhex and Zfp318 and modulates glycolysis via the CD25 pathway, enabling balanced B-cell differentiation and germinal center function.