Subsequent work using models of zymosan-induced arthritis and collagen antibody-induced arthritis revealed that properdin-deficient mice after intraarticular injection of zymosan showed a Th1 phenotype in regional lymphnodes (resulting in fewer antibodies and more proteoglycan loss in joints) [36], and in the arthritic immune complex disease, less tissue damage was observed, which in part was due to a lack of complement amplification, but also due to a cellular phenotype different from wildtype [37]. This evidence concerns the gene CFP and arthritic joint disease.