It has been reported that NKT cells and B cells interact to generate Igs, including autoantibodies27,28, whereas inhibitory roles of NKT cells against autoreactive B cells have also been described29. In the present study, we showed another novel finding that the repeated administration of α-GalCer decreased glomerular immune complex deposits. Thus, the percentage of glomeruli containing immune complex deposits, as assessed by PAS staining, was significantly lower and the IgG deposition was significantly decreased in the α-GalCer group. These findings were also observed by electron microscopy. Moreover, the IgM levels produced by CpG-ODN-stimulated spleen MNCs were significantly lower. These data suggested the suppression of autoimmune responses mediated by a decrease in B cell function. The decreased TLR-9 expression of splenic macrophages in the α-GalCer group may also have been related to the improvement of kidney pathology, since TLR-9 has been implicated in the development of lupus nephritis30. Despite the alleviation of renal injuries, the administration of α-GalCer did not affect the levels of anti-dsDNA IgG Abs. However, in the present study, the levels of anti-dsDNA Abs did not correlate with the levels of proteinuria in BWF1 mice, suggesting that these autoantibodies are not pathogenetic markers. Similarly, a study using another SLE model demonstrated an improvement in skin lesions, without any changes in the levels of anti-dsDNA Abs31.