Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by high morbidity and flares. This study used oligonucleotide microarrays to identify gene expression patterns in SLE patients, revealing a distinct signature of overexpressed granulopoiesis-related and interferon (IFN)-induced genes. Using strict statistical analysis, 15 genes were found highly up-regulated in SLE patients, 14 of which are IFN targets, with one being defensin DEFA-3, a product of immature granulocytes. A more liberal analysis identified 18 additional genes, 12 of which are IFN-regulated. These findings suggest that immature granulocytes may be involved in SLE pathogenesis. High-dose glucocorticoids, a standard treatment for SLE flares, suppress the IFN signature, supporting the role of IFN in the disease. The expression of 10 genes correlated with disease activity, with the most significant correlation involving the formyl peptide receptor-like 1 protein. The study also identified a granulopoiesis signature, with genes related to granulocyte maturation and function being highly expressed in SLE patients. These genes included enzymes, bactericidal proteins, and other molecules. The presence of immature granulocytes in SLE patients was confirmed through flow cytometry and staining techniques. The study also found that the granulopoiesis signature is independent of treatment and is present in patients with immature granulocytes. The IFN and granulopoiesis signatures were found to be distinct but may overlap in some patients. The study highlights the importance of IFN in SLE pathogenesis and suggests that targeting IFN could be a potential therapeutic approach. The findings also indicate that immature granulocytes may contribute to SLE pathogenesis through the release of proteolytic enzymes and the presentation of autoantigens to autoreactive T and B cells. The study used microarray analysis to identify gene expression patterns in SLE patients and found that these patterns can predict disease activity. The results suggest that microarray analysis of blood cells can provide valuable insights into the pathogenesis of SLE and may be useful in the diagnosis and treatment of the disease.Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by high morbidity and flares. This study used oligonucleotide microarrays to identify gene expression patterns in SLE patients, revealing a distinct signature of overexpressed granulopoiesis-related and interferon (IFN)-induced genes. Using strict statistical analysis, 15 genes were found highly up-regulated in SLE patients, 14 of which are IFN targets, with one being defensin DEFA-3, a product of immature granulocytes. A more liberal analysis identified 18 additional genes, 12 of which are IFN-regulated. These findings suggest that immature granulocytes may be involved in SLE pathogenesis. High-dose glucocorticoids, a standard treatment for SLE flares, suppress the IFN signature, supporting the role of IFN in the disease. The expression of 10 genes correlated with disease activity, with the most significant correlation involving the formyl peptide receptor-like 1 protein. The study also identified a granulopoiesis signature, with genes related to granulocyte maturation and function being highly expressed in SLE patients. These genes included enzymes, bactericidal proteins, and other molecules. The presence of immature granulocytes in SLE patients was confirmed through flow cytometry and staining techniques. The study also found that the granulopoiesis signature is independent of treatment and is present in patients with immature granulocytes. The IFN and granulopoiesis signatures were found to be distinct but may overlap in some patients. The study highlights the importance of IFN in SLE pathogenesis and suggests that targeting IFN could be a potential therapeutic approach. The findings also indicate that immature granulocytes may contribute to SLE pathogenesis through the release of proteolytic enzymes and the presentation of autoantigens to autoreactive T and B cells. The study used microarray analysis to identify gene expression patterns in SLE patients and found that these patterns can predict disease activity. The results suggest that microarray analysis of blood cells can provide valuable insights into the pathogenesis of SLE and may be useful in the diagnosis and treatment of the disease.