Our findings are consistent with observations from autoimmune disease models where FRCs indirectly restrain aberrant CD4+ T cell activation via MHCII presentation of self-antigen to induce proliferation of FoxP3+ Tregs (27, 29) and de novo conversion of Tregs (39, 76, 77) in the mLNs under homeostatic conditions. This evidence concerns the gene FOXP3 and autoimmune disease.