In addition, the importance of this cytokine as a proinflammatory third signal for maturing autoreactive CD4+ and CD8+ T cell responses was evident, as diabetogenic NOD.NY8.3 CD8+ TCR transgenic mice lacking IL-1R expression were still capable of transferring T1D.87 However, when diabetogenic NOD.BDC-2.5 CD4+ T cells were transferred to IL-1R–deficient NOD mice, a delay in the onset of T1D was observed, further suggesting the importance of IL-1 to efficiently mediate autoreactive CD4+, but not CD8+, adaptive immune responses. The gene discussed is IL1A; the disease is type 1 diabetes mellitus.