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The NF-κB family member RelB is an important transcription factor that is capable of regulating diverse immune and inflammatory responses. However, its role in the regulation of Foxp3 + regulatory T cells (Tregs) in vivo is poorly defined. In this study, we demonstrated that germline deletion of Relb resulted in systemic autoimmunity, which is associated with significant accumulation of Foxp3 + Tregs in lymphoid and nonlymphoid organs. Foxp3 + Tregs from RelB-deficient mice were functional and capable of suppressing T effector cells in vitro and in vivo, but Foxp3 - T effector cells from RelB-deficient mice showed features of hyperactivation and spontaneously produced high levels of IL-2. Surprisingly, mice with conditional deletion of Relb in T cells ( Cd4  Cre  Relb  f/f mice) or specifically in Foxp3 + Tregs ( Foxp3  Cre  Relb  f/f mice) did not show signs of autoimmunity and had similar frequencies of Foxp3 + Tregs in the periphery as wild-type C57BL/6 controls. Both strains of conditional knockout mice also had a normal conventional T cell compartment. However, reconstituting Rag-1  -/-  Relb  -/- hosts with wild-type C57BL/6 bone marrow cells led to hyperactivation of T effector cells, as well as marked expansion of Foxp3 + T cells. These data suggest that the autoimmune phenotype in germline RelB-deficient mice is most likely caused by T cell-extrinsic mechanisms, and further studies are warranted to uncover such mechanisms.

Role of the NF-κB Family Member RelB in Regulation of Foxp3+ Regulatory T Cells In Vivo