For example, IL-21R blockade in NOD mice treated with T1D-relevant pMHC class II-NPs abrogated the suppression of autoantigen cross-presentation to diabetogenic CD8 + T cells in the pancreatic lymph nodes, the anti-encephalitogenic activity of EAE-relevant pMHCII-NPs in HLA-DR4-transgenic B6 mice22, and the anti-hepatogenic activity of liver autoimmune disease-relevant pMHCII-NPs in NOD.c3c4 mice23. The gene discussed is IL21R; the disease is autoimmune hepatitis.