Thus, LPS-activated B cells express high levels of TGFβ1 and their transfer into prediabetic NOD (non-obese diabetic) mice inhibits spontaneous Th1 immunity and disease progression by down-regulating T cell autoimmunity or by modulating the function of APCs (Antigen Presenting Cell) [112]. The gene discussed is TGFB1; the disease is Autoimmunity.