chimeric antigen receptor

CAR-T cell therapy has produced durable remission in hematologic malignancies including B-cell leukemia, lymphoma, and multiple myeloma.

CAR-T cell therapy has revolutionized the treatment of hematologic malignancies, resulting in durable remission of B-cell leukemia, lymphoma, and multiple myeloma.

Strategies explored to improve CAR-T function in solid tumors include optimizing receptor clustering to boost immune synapse formation, increasing ITAM number or strength, adding novel or multiple co-stimulatory domains, cytokine secretion, epigenetic reprogramming, and synthetic biology tools for tunable or logic-gated activation.

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.

CAR-T efficacy in solid tumors is limited by poor trafficking and infiltration, immunosuppressive tumor microenvironment, intratumoral metabolic competition, and tumor antigen heterogeneity or loss.

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.

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.

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)

Chimeric antigen receptors and synthetic Notch receptors are among four synthetic receptor systems at the forefront discussed in the review.

With a special focus on four synthetic receptor systems at the forefront, including chimeric antigen receptors (CARs) and synthetic Notch (synNotch) receptors

This review synthesizes cancer immunotherapy from T-cell basic science through clinical practice, including checkpoint blockade, adoptive cellular therapy, CAR-T, and neoantigen-directed approaches.

CAR-T cell therapy has produced durable remission in hematologic malignancies including B-cell leukemia, lymphoma, and multiple myeloma.

CAR-T cell therapy has revolutionized the treatment of hematologic malignancies, resulting in durable remission of B-cell leukemia, lymphoma, and multiple myeloma.

Source: Decoding signaling architectures: CAR versus TCR dynamics in solid tumor immunotherapy.

Strategies explored to improve CAR-T function in solid tumors include optimizing receptor clustering to boost immune synapse formation, increasing ITAM number or strength, adding novel or multiple co-stimulatory domains, cytokine secretion, epigenetic reprogramming, and synthetic biology tools for tunable or logic-gated activation.

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.

Source: Decoding signaling architectures: CAR versus TCR dynamics in solid tumor immunotherapy.

CAR-T efficacy in solid tumors is limited by poor trafficking and infiltration, immunosuppressive tumor microenvironment, intratumoral metabolic competition, and tumor antigen heterogeneity or loss.

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.

Source: Decoding signaling architectures: CAR versus TCR dynamics in solid tumor immunotherapy.

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.

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)

Source: Decoding signaling architectures: CAR versus TCR dynamics in solid tumor immunotherapy.

Chimeric antigen receptors and synthetic Notch receptors are among four synthetic receptor systems at the forefront discussed in the review.

With a special focus on four synthetic receptor systems at the forefront, including chimeric antigen receptors (CARs) and synthetic Notch (synNotch) receptors

Source: Programmable synthetic receptors: the next-generation of cell and gene therapies.

This review synthesizes cancer immunotherapy from T-cell basic science through clinical practice, including checkpoint blockade, adoptive cellular therapy, CAR-T, and neoantigen-directed approaches.

Source: A guide to cancer immunotherapy: from T cell basic science to clinical practice