CAR-T Cell Therapy: Structure, Mechanism of Action, Adverse Effects, and Current Challenges

Publication Details

Publication Date

10/10/2026

Volume / Issue

Vol 1, Issue 5 (2026)

Article No.

031

Journal

British Journal of Contemporary Research

DOI

https://doi.org/10.67693/BJCR-CWLLXLWQ

Received

02 Sep 2026

Views

98

Downloads

24

Abstract

The Chimeric antigen receptor T-cells are genetically modified T-cells which are used to as powerful therapeutic treatment of patients with chemotherapy-refractory/relapsed blood cancers, acute lymphoblastic leukemia, diffuse large B-cell lymphoma, follicular lymphoma and other types of cancers. In CAR-T cell therapy, the T-cells are collected from the tumor patients and prepared the CAR-T cells lies in appropriate T-cells genetically processed in laboratory conditions. By helping the CRISPR/Cas9 technique used instead of retroviral vectors to integrate the CAR gene into specific sites in the genome of T-cells. CAR-T cells are special genetically modified T-cells which wear chimeric antigen receptor (CAR) protein on its cell membrane. The composition of these CAR proteins consists of three parts such as the recognition region which consist of a single chain antibody domain. These domains are responsible for recognition and binding to specific antigen present on cancerous cell. The middle parts of these antibodies are embedded in the membrane and third parts are the internal signaling region. The single chain variant antibody (ScFv) recognition domains which have properties anti-tumor effects through the secretion of inflammatory cytokinese.g., IL-2, IFN-γ, and TNF-α, cytolytic effector function via perforin and granzyme. TNF-related apoptosis-inducing ligand, which binds to death receptors such as DR4 and DR5 on tumor cell surface to activate graft-versus tumor effect. Also, tumor cell apoptosis can be initiated via the activation of caspase-8 and the formation of death-inducing signaling complex (DISC) leading to cell death mediated by mature caspase-3 subsequent cleavage of over 500 cellular substrates as a result of Fas and Fas ligand (FasL) pathway activation.

License

This article is published under the Creative Commons Attribution 4.0 International License . Free to read, share, and adapt with attribution.