{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nPRDM1, also known as Blimp‑1, is a master transcriptional repressor that plays a critical role in driving the terminal differentiation of B cells into antibody‐secreting plasma cells. By directly silencing genes essential for B cell receptor signaling, germinal center function, and proliferation—and by recruiting chromatin‐modifying enzymes to establish repressive chromatin marks—PRDM1 enables the coordinated induction of the plasma cell genetic program. Moreover, alternative transcription initiation from internal promoters produces isoforms with altered repressive capacity, further fine‑tuning plasma cell differentiation and function."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "9"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its pivotal role in normal B cell maturation, PRDM1 functions as a tumor suppressor whose inactivation is frequently linked to lymphomagenesis. Genetic alterations—including gene truncations, splice‐site mutations, chromosomal deletions and epigenetic silencing—and microRNA‐mediated down‑regulation of PRDM1 have been described in diffuse large B‑cell lymphoma, plasmablastic lymphoma, Hodgkin lymphoma, NK‑cell neoplasms, and other lymphoid malignancies. Genome‑wide association studies have further implicated variants in the PRDM1 locus in autoimmune conditions such as systemic lupus erythematosus, and reduced PRDM1 expression has been associated with radiation‑induced secondary cancers."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "10", "end_ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond B cells, PRDM1 exerts broad regulatory functions in the immune system and beyond. It is induced downstream of cytokine‐ and STAT‑mediated signaling in T cells and NK cells, where it modulates effector functions, memory formation, and cytotoxic activity. Viral infections add yet another layer of complexity, as viral microRNAs and proteins (for example, those derived from Epstein–Barr virus or HIV) target PRDM1 to manipulate the balance between latent and lytic infection. In addition, PRDM1 influences cell cycle regulation and apoptotic pathways—through mechanisms such as repression of p53 transcription—and has been implicated in the pathogenesis of non‑lymphoid malignancies, including gliomas and certain aggressive epithelial cancers. Notably, strategies that modulate PRDM1 expression (or disrupt its regulatory network) are emerging as potential avenues to enhance adoptive immunotherapy by sustaining a less‑differentiated, more persistent T‑cell phenotype."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "24", "end_ref": "41"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Francisco Medina, Carmen Segundo, Antonio Campos-Caro, et al. 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