Studies in T1D (and later confirmed in other disease models) showed that pMHCII-NP-induced/expanded Tr1 cells suppressed the pro-inflammatory and antigen presentation capacities of local and proximal (i.e. in pancreas-draining lymph nodes) autoantigen-loaded dendritic cells (DCs) and myeloid APCs in an Interleukin-10 (IL-10)- and Tumor Growth Factor beta (TGFβ)-dependent manner. This evidence concerns the gene IL10 and type 1 diabetes mellitus.