CD9 + B Cells Induce T Follicular Helper Cell Apoptosis to Regulate Germinal Center Regression

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ABSTRACT Adenoid hypertrophy (AH) is associated with excessive proliferation of germinal center B (GC‐B) cells, yet the mechanisms underlying GC regression and termination remain poorly understood. This study used single‐cell RNA sequencing (scRNA‐seq) to profile the cellular composition of GC‐B cells in AH. A unique subset of GC‐B cells expressing CD9 was identified through comprehensive scRNA‐seq, flow cytometry, and Mass cytometry (CyToF) analyses, with subsequent studies assessing the roles of CD9 and FOXP1 in GC‐B cell differentiation and apoptosis pathways. CD9 + B cells were detected throughout GC‐B cell development and were regulated by FOXP1. These cells also exhibited activation of cell death‐related pathways, particularly during adenoid development. AH samples showed an increase in T follicular helper (Tfh) cells, accompanied by a reduction in CD9 + B cells. In Cd9 knockout mice, CD9 deficiency led to a significant decrease in serum IgG levels. Further analysis revealed that CD9 + B cells promoted Tfh cell apoptosis via pathways such as ALCAM‐CD6. CD9 + B cells may regulate GC‐B cell regression by inducing Tfh cell apoptosis, and FOXP1 may play a role in their differentiation. These findings clarify mechanisms of GC degeneration and termination, offering potential targets for AH treatment.

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