CD4 and type 1 diabetes mellitus: Hence, the increased frequency of insulin-reactive FoxP3+ Tregs in the PLN, and the enrichment of insulin-reactive cells amongst Tregs with a stable phenotype and enhanced suppressive function, may have protected Ins+alum-treated NOD mice from T1D development by reducing the activation of pathogenic CD4+ and CD8+ T cells, limiting T cell infiltration into the pancreas.