Moreover, our data also points to a central role of the PD-1 signaling pathway in the pathogenesis of SLE, and suggests that PD-1 immunomodulation, including PD-1 agonism, could be a therapeutic option to inhibit the proliferation of pathogenic autoreactive Teff cells and selectively restore Treg regulatory homeostasis in SLE. This evidence concerns the gene PDCD1 and systemic lupus erythematosus.