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Engineered T lymphocytes are a class of advanced cellular immunotherapies where a patient's or donor's T cells are genetically modified to express specific receptors, such as Chimeric Antigen Receptors (CARs) or modified T-cell receptors (TCRs), to target and eliminate diseased cells [1][2]. These "living drugs" are designed to recognize specific antigens—most notably CD19 or BCMA in hematologic malignancies—independently of or in coordination with the major histocompatibility complex (MHC) [2][4]. Upon binding to their target antigen, these cells undergo rapid proliferation and exert potent cytotoxic effects through the secretion of pro-inflammatory cytokines and the release of cytolytic granules containing perforin and granzymes [3]. While they have demonstrated remarkable efficacy in treating refractory B-cell lymphomas and leukemias, their use is often complicated by severe systemic inflammatory responses, such as cytokine release syndrome (CRS) and neurotoxicity [3][4]. Consequently, management often requires the use of secondary drugs like tocilizumab or corticosteroids to modulate the T-cell activity and mitigate life-threatening side effects [3]. Engineered T cells represent a paradigm shift in oncology, moving from small molecule or protein-based drugs to complex, autonomous cellular systems capable of long-term persistence and immunosurveillance [1][2]. This therapeutic modality is currently being expanded to treat solid tumors and autoimmune diseases, though challenges regarding the immunosuppressive tumor microenvironment and off-target effects remain [1][4].
Engineered T cells function by expressing synthetic receptors (CARs or TCRs) that bind to specific antigens on target cells, leading to T-cell activation, proliferation, and direct lysis of the target cell via the release of cytotoxic granules [2][4].
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