IFN‐γ is generally believed to be important in the autoimmune pathogenesis of type 1 diabetes (T1D). However, the development of spontaneous β‐cell autoimmunity is unaffected in NOD mice lacking expression of IFN‐γ or the IFN‐γ receptor (IFNγR), bringing into question the role IFN‐γ has in T1D. In the current study, an adoptive transfer model was employed to define the contribution of IFN‐γ in CD4⁺ versus CD8⁺ T cell‐mediated β‐cell autoimmunity. NOD.scid mice lacking expression of the IFNγR β chain (NOD.scid.IFNγRB^null) developed diabetes following transfer of β cell‐specific CD8⁺ T cells alone. In contrast, β cell‐specific CD4⁺ T cells alone failed to induce diabetes despite significant infiltration of the islets in NOD.scid.IFNγRB^null recipients. The lack of pathogenicity of CD4⁺ T‐cell effectors was due to the resistance of IFNγR‐deficient β cells to inflammatory cytokine‐induced cell death. On the other hand, CD4⁺ T cells indirectly promoted β‐cell destruction by providing help to CD8⁺ T cells in NOD.scid.IFNγRB^null recipients. These results demonstrate that IFN‐γR may play a key role in CD4⁺ T cell‐mediated β‐cell destruction.