Description
Title: Signaling from Co-Stimulatory Receptors in CAR-T Cells
Abstract: Strategies for T cell engineering have become effective immunotherapeutic modalities for the treatment of human cancer. A well-known synthetic biology strategy to re-direct a patient’s autologous T cells’ specificity toward a desired tumor antigen is chimeric antigen receptor T (CAR-T) cell therapy. Currently, the FDA has approved CAR-T therapy for the treatment of hematological cancers, such as specific types of B cell lymphoma, acute lymphoblastic leukemia (ALL), and multiple myeloma. According to the mechanism, CAR-mediated recognition of a tumor antigen causes the spread of T cell activation signals, including a co-stimulatory signal, which causes CAR-T cells to become activated, multiply, avoid apoptosis, and develop effector functions. The limited success of early iteration CAR-T cell designs without co-stimulation led to the realization of the significance of including a co-stimulatory domain in CARs. Either a CD28 or 4-1BB co-stimulatory domain is present in every CAR-T cell used in clinical trials today. In preclinical studies, the value of adding additional co-stimulatory molecules like ICOS, OX40, and CD27 as well as various combinations of multiple co-stimulatory domains is being explored. Evidence from both clinical and preclinical studies suggests that the co-stimulatory signal affects the safety and anti-tumor effectiveness of CAR-T cell therapy in a number of ways, including response kinetics, persistence and durability, and toxicity profiles. In this article, we give an overview of how prototypical receptors co-stimulate CAR-T cells and talk about new and existing methods for modifying co-stimulatory signals to improve CAR-T cell function.
Keywords: chimeric antigen receptor; T cell engineering; co-stimulation; CD28; 4-1BB; signaling; hematologic malignancies
Paper Quality: SCOPUS / Web of Science Level Research Paper
Subject: Biomolecules
Writer Experience: 20+ Years
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