Signal regulatory protein α (SIRPα), which is highly expressed on type 2 conventional dendritic cells (cDC2), and its ligand CD47 regulate the homeostasis of cDC2 in secondary lymphoid organs (SLO) and are crucial for the development of autoimmunity. However, the molecular basis for this regulation remains poorly understood. Here, we demonstrate that ablation of SIRPα or CD47 on cDCs specifically reduces terminally differentiated Notch2‑dependent cDC2 (cDC2A) in SLO. This ablation upregulated the nuclear orphan receptor Nr4a3 and increased the frequency of annexin‑V⁺ cells in cDC2A, suggesting Nr4a3‑mediated cell death in cDC2A. Sirpa/Nr4a3 double knockout (DKO) mice showed recovery of cDC2A and a reduced percentage of annexin‑V⁺ cDC2A. Furthermore, DKO mice exhibited recovery of cDC2A‑dependent follicular helper T‑cell responses. Although SIRPα-deficient mice were resistant to the development of experimental autoimmune encephalomyelitis (EAE), DKO mice exhibited normal susceptibility to EAE. Taken together, SIRPα and CD47 on cDC2 are important for the survival and homeostatic maturation of cDC2A by preventing their activation and upregulation of Nr4a3, and thereby for T‑cell–mediated immune responses, including autoimmunity.