BCR-ABL p210-specific T-cell receptor (p210-TCR) (p210-TCR)

The BCR-ABL p210-specific T-cell receptor (TCR) is a specialized immune protein that recognizes the unique neoantigen created by the fusion of the BCR and ABL1 genes, a hallmark of Chronic Myeloid Leukemia (CML) (Ochi et al., Blood, 2009). This specific TCR is restricted to MHC class II molecules, allowing it to engage CD4+ T cells, which play a pivotal role in coordinating the immune response against leukemic cells (Yasukawa et al., Blood, 2001). Upon binding to the p210 fusion peptide presented on the cell surface, the TCR initiates signaling that leads to T-cell activation, cytokine production, and the enhancement of cytotoxic T-cell activity (Tanaka et al., J Immunother, 2012). In the landscape of modern immunotherapy, this TCR is a primary component of TCR-engineered T-cell (TCR-T) therapies designed to target minimal residual disease in patients who may not achieve a complete molecular response with tyrosine kinase inhibitors. The therapeutic application of this TCR is highly dependent on the patient's HLA profile, as the receptor only recognizes the p210 peptide when presented by specific MHC class II alleles. Research into these receptors aims to provide a curative approach by leveraging the body's own immune system to achieve long-term remission in Philadelphia chromosome-positive malignancies.

Other names

P210-specific T-cell receptorBCR-ABL fusion-specific T-cell receptorp210-MHC class II-restricted TCRp210 BCR-ABL-specific T-cell receptor

The TCR specifically binds to the p210 BCR-ABL fusion peptide presented by MHC class II molecules (e.g., HLA-DRB1*09:01), triggering CD4+ T-cell activation and an anti-leukemic immune response (Ochi et al., Blood, 2009). This binding event initiates a signaling cascade through the CD3 complex, leading to the secretion of effector cytokines like IFN-gamma and TNF-alpha to eliminate Philadelphia chromosome-positive cells (Tanaka et al., J Immunother, 2012).