Human leukocyte antigen A*24 (HLA-A*24) (HLA-A*24)

Human leukocyte antigen A*24 (HLA-A*24) is a specific allele group of the Major Histocompatibility Complex (MHC) Class I molecules, which are essential for the adaptive immune system's ability to recognize and eliminate infected or malignant cells [Wikipedia, 2024; UniProt, 2024]. It functions by binding and presenting endogenous peptides, derived from intracellular proteins, to the T-cell receptors (TCR) of CD8+ cytotoxic T lymphocytes [Cancer Sci, 2007]. HLA-A*24 is particularly prevalent in East Asian and Oceanic populations, making it a primary focus for personalized cancer immunotherapies, such as peptide vaccines and TCR-engineered T-cell therapies, in these regions [JAMA Network Open, 2023; PatSnap, 2024]. Beyond oncology, this molecule is associated with susceptibility to various autoimmune disorders like Type 1 Diabetes and Systemic Lupus Erythematosus, and plays a role in the immune response to viral infections like Hepatitis B [NIH, 2023; NIH, 2004]. Clinically, HLA-A*24:02 is a critical biomarker for identifying patients at high risk for severe cutaneous adverse drug reactions (SCARs), such as Stevens-Johnson Syndrome, in response to aromatic antiepileptic drugs like Carbamazepine and Lamotrigine [Medicine (Baltimore), 2020; Neurology, 2017]. Consequently, HLA typing is a standard procedure for both selecting eligible patients for HLA-restricted therapies and ensuring pharmacological safety in susceptible populations.

Other names

HLA-A24HLA-A*24:02HLA-A9MHC class I antigen HLA-A24HLA-A2402HL-A9

HLA-A*24 functions by binding and presenting specific 8-11 amino acid peptides to the T-cell receptor (TCR) of CD8+ cytotoxic T lymphocytes (CTLs). In cancer immunotherapy, synthetic epitope peptides (vaccines) are administered to induce a CTL response against tumor cells expressing the target antigen [Cancer Sci, 2007]. In drug hypersensitivity, certain drugs or their metabolites interact with the HLA-A*24 molecule via the hapten, p-i, or altered peptide models, leading to inappropriate T-cell activation and systemic inflammatory responses [Medicine (Baltimore), 2020; Pharmacogenomics, 2021].