This research identifies a unique plasticity state in germinal center B cells that is temporarily triggered by T follicular helper (TFH) cells. Under normal conditions, these B cells undergo extensive epigenetic remodeling to adapt their function, yet they remain susceptible to malignant transformation. The study demonstrates that this flexible state, while necessary for a healthy immune response, can be hijacked by lymphoma mutations to promote aggressive disease. Specifically, the loss of histone H1 or mutations in BTG1 allow B cells to bypass standard developmental barriers, adopting stem-like characteristics. Clinical data suggests that patients whose tumors maintain this stem-like signature face significantly poorer survival outcomes. Consequently, the findings suggest that the very mechanisms enabling immune adaptability also create a pathological window for cancer development.

References:

• Scourzic L, Izzo F, Teater M, et al. T follicular helper cells transiently unlock a plasticity state in germinal centre B cells during the humoral immune response[J]. Nature Cell Biology, 2025: 1-14.