A T Cell-B Cell Tumor-Suppressive Axis in the Germinal Center

TNFRSF14, encoding the receptor HVEM, is frequently mutated in germinal center (GC)-derived B cell lymphomas. In this issue, Mintz et al. demonstrate that the HVEM-BTLA axis restrains T cell help to GC B cells. Mutation-associated loss of this interaction promotes B cell proliferation through exaggerated T cell help, explaining how HVEM loss contributes to GC lymphomagenesis and revealing a cell-extrinsic tumor-suppressor role for BTLA.