Therefore, the aim of this study was to determine whether, in the genetic absence of properdin, the systemic and organ specific inflammation was less severe, by using a novel mouse model generated by crossing the repository archived lupus-prone MRL/MpJ-Faslpr/J mice with our line of properdin knock-out mice to produce a strain of lupus-prone properdin-deficient (MRL/lpr PKO) mice, and lupus-prone properdin-sufficient littermates (MRL/lpr PWT) as controls. This evidence concerns the gene CFP and systemic lupus erythematosus.