Our study has several limitations. It has been reported that BWF1 mice are superior to other SLE models in that they resemble the human disease, and therefore, are most commonly used42. Indeed, these mice spontaneously develop lupus nephritis-like renal lesions. However, the renal disease observed in these mice does not fully recapitulate that in humans; for example, hematuria was not observed in BWF1 mice despite proliferative glomerulonephritis. The role of NKT cells in the progression of human lupus nephritis also remains to be resolved using α-GalCer. This is partly because human NKT cells, which express T cell receptors encoded by the Vα24Jα18 and Vβ11 genes and respond to α-GalCer, are rare in the liver as well as other organs. In addition, decreased levels of human CD56+ T cells, which are not activated by α-GalCer but have been proposed as a functional counterpart for mouse NKT cells8,43,44, might be associated with high levels of serum IgG and anti-dsDNA Abs in patients with SLE14, suggesting that CD56+ T cells may ameliorate SLE. Therefore, it should be carefully evaluated in the future whether human NKT cells or CD56+ T cells are really involved in lupus nephritis.