Dendritic cells (DCs) survey peripheral tissues in an immature, antigen-sampling state but execute their antigen-presenting function as mature cells in the lymph node (LN). DC maturation occurs in response to immunogen recognition and involves upregulation of the chemokine receptor CCR7, migration to regional LNs, and antigen presentation to T cells. In the steady state, DCs undergo a similar program of homeostatic maturation and migration but present self-antigen to regulatory T cells (Treg), a process necessary to maintain tolerance. Our studies established the transcriptional repressor Etv3 as a master regulator of this tolerogenic function of mature DCs during homeostatic maturation. Etv3 is upregulated during homeostatic maturation and coordinates this program at the chromatin, transcription, and protein levels. Functionally, Etv3-deficient DCs migrate less effectively in vitro and in vivo, fail to maintain Treg, and drive spontaneous autoimmunity in a dominant manner. However, it is unclear whether the Etv3-dependent migratory program is mechanistically linked to the tolerogenic program that maintains Treg. To address this question, we performed immunofluorescence confocal imaging of steady-state LNs from wild-type, Etv3-deficient, and Etv3-reporter mice. Preliminary studies indicate that Etv3-expressing mature DCs co-localize with Treg in the T cell zones of LNs. Etv3-deficient mature DCs show aberrant positioning in the LN and reduced interaction with Treg. These emerging data support a working model in which an Etv3-mediated homeostatic program facilitates mature DC–Treg co-localization in the LN to promote peripheral tolerance.