The key advantage of the system is the adaptor molecule, often an antibody-based reagent, that targets the TAA.
First-pass extracted concept
adaptor molecule
Aliases
AM
Evidence Snippets
Supporting Sources
Linked Claims
Modular CAR T-cell effector function is activated only when the CAR, adaptor molecule, and antigen-positive target cell assemble correctly.
Only when the CAR, AM, and antigen-positive target cell assemble correctly is T-cell effector function activated, leading to cancer cell lysis.
Adaptor molecules can be swapped or combined without re-engineering the T cells, enabling multiplexing and logic-gated control.
Adaptors can be swapped or combined without re-engineering the T cells, enabling straightforward multiplexing and logic-gated control.
Adaptor architecture, especially size, affects pharmacokinetics and therefore adaptor dosing schemes in modular CAR systems.
And lastly, the architecture of the AM, especially the size, defines the pharmacokinetics and, consequently, the dosing scheme of the AM.
Adaptor valency affects exhaustion and non-specific activation of modular CAR T cells.
Third, the valency of the AM has an impact on exhaustion and non-specific activation of CAR T cells.
The affinities of CAR-adaptor and adaptor-antigen interactions mostly define engagement kinetics in modular CAR systems.
Second, the affinity of CAR-AM and AM-TAA will mostly define the engagement kinetics of the system.
Modular CAR T cells use a two-part system in which the CAR binds an adaptor molecule and the adaptor binds the tumour-associated antigen.
Modular CAR T cells use a two-part system: the CAR on the T cell binds an adaptor molecule (AM), and that adaptor binds the tumour-associated antigen (TAA).