ArticleBlood advances2026
CD20 bispecific T-cell engager depletes B-cell progenitors preventing EBV-associated lymphomagenesis in humanized mice.
Article in Blood advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
abstractEpstein-Barr virus (EBV) infection is associated with ∼1.5% of human tumors, including B-cell lymphoproliferative diseases (LPDs). A common approach to treating EBV-associated LPDs is targeting infected tumor cells with a CD20 monoclonal antibody, such as rituximab, although this often fails to prevent relapses and refractory disease. In this study, we show using a preclinical humanized mouse model the superior efficacy of a CD3×CD20 bispecific T-cell engager in preventing systemic virus spread and EBV-associated tumor formation, compared with rituximab treatment. This increased efficacy is associated with a deep depletion of human precursor B cells in the bone marrow. Progenitor B cells are permissive to infection with EBV in vitro and correlate with EBV persistence during B-cell depletion therapy, also in vivo. Thus, deep depletion of B cells, including bone marrow progenitors, might target EBV-associated LPDs more efficiently. Infected progenitors should be considered an EBV reservoir from which associated pathologies could relapse.
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