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Interferon and Granulopoiesis Signatures in Systemic Lupus Erythematosus Blood

Lynda Bennett^1,2, A. Karolina Palucka¹, Edsel Arce^1,2, Victoria Cantrell^1,2, Josef Borvak¹, Jacques Banchereau¹ and Virginia Pascual^1,2

¹ Baylor Institute for Immunology Research, Dallas, TX 75204
² The University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390

Address correspondence to V. Pascual or J. Banchereau, Baylor Institute for Immunology Research, 3434 Live Oak, Dallas, TX 75204. Phone: 214-820-7450; Fax: 214-820-4813; E-mail: virginip{at}baylorhealth.edu or jacquesb{at}baylorhealth.edu

Systemic lupus erythematosus (SLE) is a prototype systemic autoimmune disease characterized by flares of high morbidity. Using oligonucleotide microarrays, we now show that active SLE can be distinguished by a remarkably homogeneous gene expression pattern with overexpression of granulopoiesis-related and interferon (IFN)-induced genes. Using the most stringent statistical analysis (Bonferroni correction), 15 genes were found highly up-regulated in SLE patients, 14 of which are targets of IFN and one, defensin DEFA-3, a major product of immature granulocytes. A more liberal correction (Benjamini and Hochberg correction) yielded 18 additional genes, 12 of which are IFN-regulated and 4 granulocyte-specific. Indeed immature neutrophils were identified in a large fraction of SLE patients white blood cells. High dose glucocorticoids, a standard treatment of disease flares, shuts down the interferon signature, further supporting the role of this cytokine in SLE. The expression of 10 genes correlated with disease activity according to the SLEDAI. The most striking correlation (P < 0.001, r = 0.55) was found with the formyl peptide receptor-like 1 protein that mediates chemotactic activities of defensins. Therefore, while the IFN signature confirms the central role of this cytokine in SLE, microarray analysis of blood cells reveals that immature granulocytes may be involved in SLE pathogenesis.

Key Words: microarray • immature granulocytes • glucocorticoid • leukocytes • autoimmunity

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• Moir, S., Malaspina, A., Pickeral, O. K., Donoghue, E. T., Vasquez, J., Miller, N. J., Krishnan, S. R., Planta, M. A., Turney, J. F., Justement, J. S., Kottilil, S., Dybul, M., Mican, J. M., Kovacs, C., Chun, T.-W., Birse, C. E., Fauci, A. S. (2004). Decreased Survival of B Cells of HIV-viremic Patients Mediated by Altered Expression of Receptors of the TNF Superfamily. JEM 200: 587-600 [Abstract] [Full Text]  
• Hron, J. D., Peng, S. L. (2004). Type I IFN Protects Against Murine Lupus. J. Immunol. 173: 2134-2142 [Abstract] [Full Text]  
• Barnes, M. G., Aronow, B. J., Luyrink, L. K., Moroldo, M. B., Pavlidis, P., Passo, M. H., Grom, A. A., Hirsch, R., Giannini, E. H., Colbert, R. A., Glass, D. N., Thompson, S. D. (2004). Gene expression in juvenile arthritis and spondyloarthropathy: pro-angiogenic ELR+ chemokine genes relate to course of arthritis. Rheumatology (Oxford) 43: 973-979 [Abstract] [Full Text]  
• Jury, E C, Kabouridis, P S (2004). T-lymphocyte signalling in systemic lupus erythematosus: a lipid raft perspective. Lupus 13: 413-422 [Abstract]  
• Blasius, A., Vermi, W., Krug, A., Facchetti, F., Cella, M., Colonna, M. (2004). A cell-surface molecule selectively expressed on murine natural interferon-producing cells that blocks secretion of interferon-alpha. Blood 103: 4201-4206 [Abstract] [Full Text]  
• Sharif, M. N., Tassiulas, I., Hu, Y., Mecklenbrauker, I., Tarakhovsky, A., Ivashkiv, L. B. (2004). IFN-{alpha} Priming Results in a Gain of Proinflammatory Function by IL-10: Implications for Systemic Lupus Erythematosus Pathogenesis. J. Immunol. 172: 6476-6481 [Abstract] [Full Text]  
• Castellano, G., Woltman, A. M., Nauta, A. J., Roos, A., Trouw, L. A., Seelen, M. A., Schena, F. P., Daha, M. R., van Kooten, C. (2004). Maturation of dendritic cells abrogates C1q production in vivo and in vitro. Blood 103: 3813-3820 [Abstract] [Full Text]  
• Utz, P J (2004). Multiplexed assays for identification of biomarkers and surrogate markers in systemic lupus erythematosus. Lupus 13: 304-311 [Abstract]  
• Schmidt, K N, Ouyang, W (2004). Targeting interferon-{alpha}: a promising approach for systemic lupus erythematosus therapy. Lupus 13: 348-352 [Abstract]  
• Looney, R J, Anolik, J, Sanz, I (2004). B lymphocytes in systemic lupus erythematosus: lessons from therapy targeting B cells. Lupus 13: 381-390 [Abstract]  
• Prokunina, L., Alarcon-Riquelme, M. (2004). The genetic basis of systemic lupus erythematosus--knowledge of today and thoughts for tomorrow. Hum Mol Genet 13: R143-148 [Abstract] [Full Text]  
• Yang, J.-Q., Singh, A. K., Wilson, M. T., Satoh, M., Stanic, A. K., Park, J.-J., Hong, S., Gadola, S. D., Mizutani, A., Kakumanu, S. R., Reeves, W. H., Cerundolo, V., Joyce, S., Van Kaer, L., Singh, R. R. (2003). Immunoregulatory Role of CD1d in the Hydrocarbon Oil-Induced Model of Lupus Nephritis. J. Immunol. 171: 2142-2153 [Abstract] [Full Text]  
• Hardin, J. A. (2003). Directing Autoimmunity to Nucleoprotein Particles: The Impact of Dendritic Cells and Interferon {alpha} in Lupus. JEM 197: 681-685 [Full Text]  

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