Importantly, adipocyte- or macrophage-specific depletion of MHC II in obese mice reduces CD4+ T cell numbers (especially the effector/memory CD4+ T cells) and IFN-γ production in VAT and improves insulin sensitivity, indicating critical roles of MHC II on adipocytes or macrophages in adipose tissue Th1 polarization, which contributes to obesity-induced adipose tissue inflammation and insulin resistance (40, 56, 63). The gene discussed is CD4; the disease is Insulin resistance.