Dendritic cell (DC) expression of the immune checkpoint molecule CTLA-4 plays a critical role in shaping T cell polarization and the efficacy of DC-based immunotherapies, yet the transcriptional mechanisms governing DC CTLA-4 expression remain poorly defined. Here, we identify a polarization-responsive transcriptional rheostat in which GATA3 activates, and C/EBP-β represses, CTLA-4 transcription in DCs. Maturation and type 2–associated signals upregulate both GATA3 and CTLA-4 at the mRNA and protein levels. GATA3 directly promotes CTLA-4 transcription, as demonstrated by promoter occupancy and luciferase reporter assays, and ChIP-seq analysis reveals binding at a distal enhancer-associated region, suggesting multi-site regulation. In contrast, C/EBP-β, which is highly expressed in immature DCs, directly binds the CTLA-4 promoter and suppresses transcription. Luciferase assays demonstrate that C/EBP-β isoforms dynamically regulate CTLA-4 expression through dominant negative inhibition. Notably, C/EBP-β exerts epistatic control over this axis by restraining GATA3 expression, thereby coupling DC polarization state to CTLA-4 output. Both GATA3 and C/EBP-β are responsive to maturation and polarization cues, enabling graded control of CTLA-4 expression across DC states. Together, these findings define a tunable transcriptional mechanism linking DC polarization programs to immune checkpoint regulation, with implications for the rational design of DC-based immunotherapies.