It was demonstrated that C5aR- and FcγR activation on neutrophils were necessary for the initiation and progression of arthritis, and that C5aR activation of neutrophils was required for their LTB4 release, while FcγR engagement mediated IL-1β release (35) (complement activation is discussed below and in Figure 2). This evidence concerns the gene FCGR2A and arthritic joint disease.