TLR7 and systemic lupus erythematosus: CD22 deficiency however does accelerate the development of autoimmunity in autoimmune-susceptible mice, Mary at al. showed that crossing CD22−/− mice onto mice carrying the Yaa locus, which predisposes mice to develop lupus-like disease due to duplication of TLR7 and other genes, significantly increased auto-Ab production (70).