<i>Tet2</i> deficiency promotes IgG1+ B-cell expansion and differentiation blockade through deregulation of the <i>Nfkbia</i>-c-Rel axis.

ABSTRACT: The germinal center (GC) reaction is essential for orchestrating humoral immunity by producing plasma cells (PCs) and memory B cells (MBCs). TET2, an α-ketoglutarate-dependent dioxygenase, plays a critical role in B-cell exit from the GC and in plasma cell differentiation. Moreover, TET2 functions as a tumor suppressor in diffuse large B-cell lymphoma (DLBCL), with mutations frequently observed in the ST2 DLBCL subgroup, which is marked by elevated NF-κB and PI3K signaling and predominant expression of IgG B-cell receptors (BCRs). We used a combination of in vivo mouse models and in vitro differentiation systems to investigate the effects of Tet2 deficiency on IgG1+ GC B-cells. We performed flow cytometry, gene expression, and DNA methylation analysis to assess differentiatio

SUBMITTER: Ghamlouch H 

PROVIDER: S-EPMC12797087 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature