In conclusion, we found that IL-22 secreted mainly by local ILC3s acted on kidney cells to enhance STAT3 phosphorylation and over-expression of CCL2 and CXCL10, thus promoting infiltration of macrophages into the kidney and then aggravating LN, and that IL-22 or IL-22R KO delayed the disease development of lupus-prone mice. Here, CCL2 is linked to systemic lupus erythematosus.