ArticleMolecular therapy. Oncology2026
ICAM1-targeted costimulation extends HER2 CAR T cytotoxicity to HER2-low and HER2-negative tumors through synergy with TCR signaling.
Article in Molecular therapy. Oncology, 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
Autologous T cells engineered to express a HER2 chimeric antigen receptor (CAR) have shown limited clinical efficacy. To broaden antitumor activity, we co-expressed a chimeric costimulatory receptor (CCR) targeting ICAM1 (ICCR) in HER2 CAR T cells. ICAM1 is upregulated by inflammatory cytokines, reinforces immune-synapse formation, and is elevated in aggressive or dedifferentiated tumors, including those with heterogeneous or low HER2 expression. HER2 CAR/ICCR T cells preserved potent cytotoxicity against HER2-high targets and showed significantly enhanced killing of HER2-low cell lines compared with HER2 CAR T cells alone. ICCR augmented NF-κB activation particularly under low HER2 conditions. Upon repeated stimulation with HER2-negative tumor cells, HER2 CAR/ICCR T cells underwent nearly 10-fold expansion with superior cytotoxicity, whereas HER2 CAR T cells failed to expand.
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