More recently, the complement system has been found to exhibit a dynamic interplay with neutrophils in the pathogenesis of SLE, the crosstalk facilitated by the presence of complement receptors on the surface of neutrophils including complement receptor 1 (CR1), C3a receptor (C3aR) and C5a receptor 1 (C5aR1) (109). This evidence concerns the gene CR1 and systemic lupus erythematosus.