ReviewActa biochimica et biophysica Sinica2026
Decoding signaling architectures: CAR versus TCR dynamics in solid tumor immunotherapy.
Review in Acta biochimica et biophysica Sinica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- CAR-T cell therapy in cancer immunotherapy - Biology, clinical successes, and emerging challenges: A review.Biomolecules & biomedicine · 2026Review
- Special issue: advances in immunology and its applications.Acta biochimica et biophysica Sinica · 2026Article
- Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The T cell receptor (TCR) initiates signaling by specifically recognizing peptide-MHC complexes, triggering the phosphorylation of CD3 chain immunoreceptor tyrosine-based activation motifs (ITAMs). This recruits kinases such as ZAP70, triggering a tightly regulated signaling cascade that governs T cell activation, differentiation, and effector functions. In contrast, the chimeric antigen receptor (CAR) is a synthetic construct that bypasses MHC restriction by fusing an antigen-binding domain with intracellular signaling modules (usually CD3ζ and co-stimulatory domains) from the TCR complex and other receptors. CAR-T cell therapy has revolutionized the treatment of hematologic malignancies, resulting in durable remission of B-cell leukemia, lymphoma, and multiple myeloma. However, its efficacy in solid tumors is limited by intrinsic barriers: poor CAR-T-cell trafficking/infiltration into tumors, the immunosuppressive tumor microenvironment (TME), intratumoral metabolic competition, and tumor antigen heterogeneity/loss. To improve CAR-T-cell function in solid tumors, numerous studies have explored multiple strategies: engineering CARs to boost immune synapse formation via optimized receptor clustering, increasing the ITAM number/strength to amplify downstream signaling, and incorporating novel/multiple co-stimulatory domains to sustain T-cell activation and persistence. Additionally, approaches include the use of CAR-T cells that secrete pro-inflammatory cytokines, epigenetic reprogramming to preserve T-cell stemness and functionality, and the use of synthetic biology tools for tunable/logic-gated CAR activation. Here, we summarize the current understanding of CAR signaling dynamics and highlight recent breakthrough strategies designed to overcome these challenges in solid tumors. These advances narrow the liquid-solid tumor efficacy gap, holding promise for better clinical outcomes in patients with solid malignancies and a new era of personalized immunotherapy.
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Registered trials
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