Downregulation of CD200R1 in SLE may contribute to impaired generation of regulatory signals, and increased production of CD200 in vivo could bind to other receptors such as CD200R2 to CDR200R4 [14], thereby transmitting stimulatory signals leading to the enhanced differentiation of Th17 cells, as has been reported [43]. The gene discussed is CD200R1L; the disease is systemic lupus erythematosus.