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Anti-thymocyte globulin (ATG) refers to a complex therapeutic target profile consisting of multiple T-lymphocyte surface antigens, including CD2, CD3, CD4, CD8, CD11a, CD18, CD25, CD44, and CD45, as well as HLA class I and II molecules (Mohty, 2002). It is a polyclonal antibody preparation produced by immunizing animals, typically rabbits or horses, with human thymocytes or T-lymphoblastoid cell lines (Popow et al., 2013). The primary biological function of targeting these antigens is to induce profound immunosuppression through the rapid depletion of circulating T-cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis (Zand et al., 2005). Beyond depletion, ATG interferes with T-cell activation, adhesion, and trafficking by blocking various surface receptors (Mohty, 2002). Clinically, it is a cornerstone therapy for preventing and treating acute cellular rejection in solid organ transplantation and is a standard treatment for severe aplastic anemia (FDA, 2017). Due to its polyclonal nature, it also exhibits lower-level binding to other blood cells, such as platelets and neutrophils, which can lead to hematologic side effects (Bourdage & Hamlin, 1995).
Induces T-cell depletion through complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), and apoptosis, while also modulating cell surface receptors involved in T-cell activation, adhesion, and trafficking.
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