Taken together, these results suggest again the existence of qualitative differences among circulating CD3+-Ex depending on the status of parental T-cells, and point out IFN-signaling and activation of senescent CD4+ T-cells as underlying factors of the chronic immune activation and excessive cytokine/chemokine response occurring in SLE, aberrant CD3+-Ex being significant mediators. This evidence concerns the gene IFNA1 and systemic lupus erythematosus.