These results indicate that the MRL/MpJ-Faslpr/J murine model shows an accumulation of cDC CD103−CD11b+ MHC-II+ cells, an increase in ICOSL expression in the spleen during week 16 of our study, in conjunction with a positive correlation between M-MDSC MHC-II and IFN-γ-producing CD4+ T cells, which could be promoting the SLE development. The gene discussed is IFNG; the disease is systemic lupus erythematosus.