Exploring the availability of PD-L1/L2 to PD-1 in SLE could yield valuable insights, potentially positioning this interaction as a promising therapeutic target during autoimmune responses, as demonstrated in a recent study that the interaction between astrocytic PD-L1 and microglial PD-1 is necessary for the attenuation of autoimmune central nervous system inflammation in the acute and progressive stages of a mouse model of multiple sclerosis [101]. This evidence concerns the gene CD274 and systemic lupus erythematosus.