ArticleCancer research2026
TLR9 Agonists Potentiate Adoptive T-cell Therapy in Cancer through a B-cell-CD2 Costimulatory Axis.
Article in Cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Dual stimulation of CD40 and 41BB pathways during ex-vivo TIL expansion enhances CD8+ T cell expansion.bioRxiv : the preprint server for biology · 2026Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Adoptive T-cell transfer (ACT) therapy offers curative potential for some patients with cancer. Toll-like receptor (TLR) agonists improve the efficacy of ACT therapy, and elucidating the underlying mechanism of potency could help determine the best way to maximize the benefits of TLR agonists. In this study, we identified an innate-adaptive circuit in which TLR9-activated B cells augment CD8+ T-cell fitness and antitumor activity through CD2-dependent costimulation. Among multiple TLR agonists tested, class B CpG uniquely programmed murine and human CD8+ T cells for superior effector differentiation, metabolic fitness, and antitumor control. Disruption of CD2 signaling blunted the benefits of TLR9 agonism, including impaired glycolytic capacity and reduced tumor control. Independently, blocking other costimulatory molecules, such as CD86, CD80, CD28, or inducible T-cell costimulator (ICOS), did not impair the antitumor activity of CpG-conditioned T cells. Gain-of-function experiments revealed that CD2 stimulation recapitulated the effect of TLR9 agonism, bolstering the effector function of tumor-infiltrating lymphocytes and chimeric antigen receptor (CAR) T cells. Consistent with these findings, elevated CD2 expression in human tumors correlated with improved overall survival across multiple patient cohorts with cancer, underscoring the clinical importance of this signaling cue. Together, these data uncover a noncanonical B-cell-CD2 costimulation axis through which TLR9 agonists potentiate ACT, revealing a targetable pathway to overcome resistance to cell therapy in solid tumors. SIGNIFICANCE: B cells activated with TLR9 agonist cross-talk with CD8+ T cells via CD2, which enhances their fitness, cytotoxic function, and antitumor activity against solid tumors.
Indexed as
Identifiers
42406997What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.