Acute myeloid leukemia-associated antigens (presented by autologous dendritic cells) (AML-LAA-DC)

Acute myeloid leukemia (AML)-associated antigens presented by autologous dendritic cells (DCs) represent a personalized immunotherapy strategy designed to eradicate residual leukemic cells and prevent relapse. This approach involves harvesting a patient's own monocytes, differentiating them into dendritic cells ex vivo, and loading them with specific AML-related proteins—such as Wilms tumor 1 (WT1), PRAME, or RHAMM—or whole leukemic cell lysates (Lichtenegger et al., 2017). These matured DCs are then re-administered to the patient, where they migrate to lymphoid organs and present the antigens to naive and memory T cells via MHC molecules (Anguille et al., 2012). This process triggers the expansion of leukemia-specific cytotoxic T lymphocytes (CTLs) capable of recognizing and killing AML blasts. By utilizing the patient's own immune machinery, this therapy aims to provide a durable anti-tumor surveillance mechanism, particularly in the setting of minimal residual disease (MRD). Clinical trials have demonstrated that this modality is generally well-tolerated, with a low risk of severe systemic toxicity compared to traditional chemotherapy (Van de Velde et al., 2009). The antigens themselves serve as the molecular targets for the induced T-cell response, while the autologous dendritic cells act as the delivery and activation vehicle. This strategy is often explored as a maintenance therapy to prolong complete remission in AML patients who are at high risk of recurrence.

Other names

AML tumor-associated antigensLeukemia-associated antigensLAADC-presented AML antigensAutologous DC-loaded antigens

Induction of a specific T-cell mediated immune response against leukemic blasts through the ex vivo loading and subsequent in vivo presentation of tumor-associated antigens by mature autologous dendritic cells (Anguille et al., 2012).