The disorder of B cells is one of the hallmarks of systemic lupus erythematosus (SLE).The activation state indicated by CD86 of B cells from SLE is well known,while the defect of regulatory B cells mediated by CD1d is also responsible for the process of SLE.In the present study,we focused on the relationship between B cell activation mediated by CD86 and B cell regulatory function mediated by CD1d.Our results showed that the level of CD1d in B cells was decreased during the early stages of B6.MRLIpr SLE mice and imiquimod-treated (IMQ-treated) mice,while the level of CD86 was significantly increased at the late stage.Moreover,the expression of CD1d showed a significantly negative correlation with CD86 level in B cells from IMQ-treated mice (r =-05741;P =0.0022),B6.MRLIpr mice (r =-0.7091;P =0.0268),and SLE patients (r =-0.4125;P =0.0404).The in vivo and in vitro experiments with splenocytes demonstrated that CD1d signaling pathway could inhibit toll-like receptor 7 (TLR7)-induced CD86 expression of B cells.Further studies showed that this relationship also affected antibody production.Thus,our results confirmed the association of CD1d and CD86 levels in B cells from SLE,and demonstrated the importance to preserve the immunoregulatory function of B cells mediated by CD1d in the progression of SLE.