Prdm1, also known as BLIMP1, is a key transcription factor. It plays important roles in cell differentiation, immune regulation, and cancer-related processes. In B cells, it acts as a master regulator of plasma cell differentiation; in T cells, it is crucial for terminal effector cell differentiation [2]. It is also involved in pathways related to cancer immune evasion and T-cell hyporesponsiveness. Genetic models, especially KO/CKO mouse models, are valuable for studying Prdm1.

In a Ncr1-driven conditional knockout mouse model, Prdm1 was shown to regulate the composition and maturation of cNK cells in the liver. Prdm1-deficient cNK cells and liver ILC1s had decreased secretion of interferon-γ, granzyme B, and perforin, leading to increased cancer metastasis [3]. Genetic knockout of Prdm1 in antitumor T cells by Nuclease technology supported the maintenance of an early memory phenotype and polyfunctional cytokine secretion in repeatedly stimulated CAR-engineered T cells, enhancing T-cell persistence and therapeutic efficacy in multiple tumor models [1].

In conclusion, Prdm1 is essential for cell differentiation in B and T cells and significantly impacts immune-related processes. Studies using KO/CKO mouse models have revealed its role in cancer metastasis, T-cell-based immunotherapy, and immune surveillance, providing insights into potential therapeutic strategies for liver cancer and adoptive cancer immunotherapies.